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Antibiotics Flashcards

1
Q

what is an infection

A

invasion of the body by various microorganisms: bacteria, fungus, protozoans, viruses, and worms- and the associated reaction of the body to them

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2
Q

how are bacterial infections treated

A

with antibiotics after appropriate diagnosis

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3
Q

pathogen identification requires

A

culturing and other laboratory work…time and money

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4
Q

what is empiric therapy

A

practical and necessary with life threatening cases but also has significant potential problems

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5
Q

drug resistance due to

A

USE and exacerbated by misuse of antibiotics

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6
Q

clinical diagnosis include

A
  • symptoms of infection
  • physical exam
  • patient history
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7
Q

clinical lab test include

A

microbiological diagnosis

  • gram stain analysis
  • identify the unique peptidoglycan cell wall of bacteria
  • differentiates bacteria as: gram +, gram -(+) or gram -, gram-(-)
  • antibody screening, others: x-ray
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8
Q

what type of wall does gram-(+) bacteria have

A
  • many layers peptidoglycan (90% of wall)

- a polymer composed of polymerized sugar (polysaccharide) and peptide chains connected by amino acid bridges

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9
Q

what type of wall does gram-(-) bacteria have

A
  • much thinner peptidoglycan layer (only 20% of the wall); associated with an OM periplasmic space, and lipopolysaccharide layer
  • cell wall is not regulatory structure like cell membrane; it is not selectively permeable
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10
Q

what are bactericidal antibiotics

A

destructive to bacteria, concentration-dependent killing or time-dependent killing

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11
Q

what are bacteriostatic antibiotics

A

inhibit the growth or multiplication of bacteria, let the immune system eradicate them

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12
Q

what is pharmacokinetics

A

absorption, distribution, and drug elimination

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13
Q

when selecting antibiotics what should you consider

A
  • adverse effects
  • drug interaction
  • resistance
  • post antibiotic effects
  • contraindications: not given during pregnancy, to children, elders, or others (liver, kidney, allergy)
  • multiple antibiotic therapy:polymicrobial infections, etc
  • cost of therapy
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14
Q

what bacteria pathogens are susceptible

A

gram-(+) and gram -(-); cocci, bacilli, clostridium, mycobacterium, bacteroides

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15
Q

what Chlamydia pathogens are susceptible

A

gram-(-), spherical microorganisms

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16
Q

what Spirochete pathogens are susceptible

A

gram-(-), flexible, sprial-shaped

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17
Q

what mycoplasma pathogens are susceptible

A

smallest free-living microorganisms

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18
Q

how do bacteria become resistant to antibiotics

A
  1. antibiotic fails to reach its target
  2. antibiotic is inactivated
  3. target is altered
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19
Q

how do antibiotics fails to reach its target

A

some bacteria have impermeable membrane for the drug (lack of transport system or reduced porins)

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20
Q

how are antibiotic is inactive

A

bacteria produce enzyme destruction (eg. B-lactamases destroy the B-lactam ring of penicillins), or metabolism of the drug

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21
Q

how is the target altered

A

due to down-reguation of porin, and drug mutation of transpeptidase, reduced drug access elimination by energy-depdendent efflux, etc

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22
Q

efflux pumping causes

A
  1. resistance to antibiotics by mutation may be transmitted via plasmids or chromosomal DNA
  2. alternative pathways…other mechanisms
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23
Q

what are the die hard bacteria

A 
Methicillin-resistant staphylococcus aureus
Pseudomonas Aeruginosa
Vancomycin-resistant enterococci
Clostridium
Enterobacteriacea
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24
Q

Methicillin-resistant staphylococcus aureus (MRSA) “golden staph” is the major cause of

A

nosocomial infection

-cause illnesses from minor skin infections to life-threatening pneumonia, meningitis, endocarditis, and septicaemia

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25
what type of bacteria is Pseudomonas aeruginosa
gram-(-), aerobic
26
pseudomonas aerguinosa is a major cause of
hospital infections | -prevalent among patients with burn wounds, acute leukemia, IV drug additions
27
what type of bacteria is Vancomycin-Resistant Enterococci
gram-(-) anaerobic
28
what type of bacteria is Clostridium
gram- (+), anaerobic, produces destructive exotoxins
29
what type of baxter is enterobacteriaceae
gram-(-), anaerobic, can cause fatal abscesses and bacteremias
30
what are the bacteria cell wall synthesis inhibitors
1. penicillins "-cillin" 2. cephalosporins "cef~1-4th gen" 3. carbapenems and monobactam 4. others: vancomycin, bacitracin, fosfomycin & cycloserine
31
mechanism of bacteria cell wall synthesis inhibitors
mechanism of protein synthesis in micoorganisms are not identical to those of mammalian cells - bacteria have 70s ribosomes, whereas mammalian cells have 80s ribosomes - differences exist in ribosome subunits and in the chemical composition and functional specificities of component nucleic acids and proteins - such difference form the basis for the selective toxicity of these drugs against microorganisms
32
what are the B-lactam antibiotics
penicillins: - penicillin G - penicillin V - Oxacillin - Dicloxacillin - Ampicillin - Amoxicillin - Ticarcillin - Mezlocillin
33
what is the structure of penicillin
- penicillins contain a thiazolidine ring (a) and a B-lactam ring (b) - A side-chain of penicillin (R) can be added to 6-aminopenicillanic acid with action of amidase to form a different penicillin
34
what is penicillin G
- the only natural penicillin | - used in the form of benzathine, procaine, potassium & sodium salts
35
what is penicillin V
semi-synthetic
36
what are the narrow spectrum penicillins
- oxacillin | - dicloxacillin
37
what are the broad-spectum pencillins
- ampicillin (amino pencillins) - amoxicillin (amino penicillin) - ticarcillin (carboxy penicillins) - mezlocillin (acylureido penicillins)
38
define bactericidial
kill bacteria
39
define bacteriostatic
inhibit microbial growth
40
define beta-lactam antibiotics
drugs with structures containing a beta-lactam ring
41
what is MIC
lowest concentration of antimicrobial drug capable of inhibiting growth of an organism
42
what is penicillin-binding proteins (PBPS)
bacterial cytoplasmatic membrane proteins that act as the initial receptors for penicillins and other beta-lactam antibiotics
43
what is peptidoglycan
chains of polysaccharides and peptides polypeptides that are cross-linked to form the bacteria cell wall
44
what is selective toxicity
more toxicity to the invader than to the host
45
what is transpeptidases
bacterial enzymes involved in the cross-linking of linear peptidoglycan chains, the final step in cell wall synthesis
46
penicillins and cephalosporins are the major antibiotics that inhibit
- bacterial cell wall synthesis | - inhibit the synthesis of peptidoglycan (PG) by inhibiting transpeptidase (transpeptidation)
47
what are the antimicrobials are narrow spectrum
-natural penicillin (G) -semisynthetic penicillin V -anti-staphylococcal pencillins: Isoazolyl penicillins: Oxacillin Dicloxacillin
48
what are the antimicrobials that are broad spectrum
``` amino penicillins (ampicillin, amoxicillin) Carboxy penicillins (ticarcillin) Acyleureido penicillins (mezlocillin) ``` - bactericidal (if bacteria are growing and dividing) - effective for gram-(+), some gram-(-) and anaerobes
49
what are the clinical uses of antimicrobials
1. septicicemia 2. meningitis 3. hospital-acquired (bacterial) penumonia 4. cellulitis 5. bone and joint infections 6. acute/chronic urinary tract infections
50
how does resistance to antimicrobials occur
1. inactivation by bacterial B-lactamases 2. mutant transpeptidases 3. down-regulation of porins 4. efflux pump
51
inactivation by bacterial B-lactmase is most common in what bacteria
Staphylococcus aureus Pseudomonas aeruginosa E.coli enterobacters
52
what is mutant transpeptidases
alterations in the drug targeted Penicillin binding proteins, reduce the affinity for drug binding in staphylococci, pneumococci and enterococci
53
effects of down-regulation of porins
impairs drug penetration via porins in gram-(-) bacteria
54
pharmacokinetics of antimicrobials
poor oral absorption, except: Penicillin V - Isoxazolyl penicillins (oxacillin, dicloxacilllin), Amino penicillins (ampicillin, amoxicillin) -variable distribution throughout the body, do not enter the CNS unless there is inflammation -not metabolized and generally excreted by the kidney
55
what are the adverse rxns of antimicrobials
- hypersensitivity/allergic rxns (1-5%) may cause anaphylactic shock - GI distress: nausea, vomiting with oral high doses (not to be mistaken as allergic run) - Seizures (with high doses) - Hypokalemia (with high doses) - superinfections: chronic use may lead to a new/secondary infection, occuring in a patient having a pre-exisitng infection
56
what are the drug interactions with penicillin
-very few; in vitro mixing with aminoglycosides reduces the activity of both
57
what is probenecid
an uricosuric agent which increases excretion of uric acid in hyperuricemia, decreases excretion of penicillins
58
describe the structure of B-lactamase inhibitors
- they have a B-lactam ring (like penicillins & cephalosporins) but lack antimicrobial activity - bind irreversible to and inhibit bacterial B-lactmases - neither bactericidal nor bacteriostatic (not antibiotics)
59
see slide 31
see slide 31
60
what is septicemia
commubity and hospital-acquired pneumonia, cellulitis, sinusitis, bone and joint infection
61
how is clavulanate absorbed
after oral administration
62
how is sulbactum & tazobactum administered
IV due to poor oral administration
63
piperacillin increases the half life of
tazobactum
64
describe the structure of cephalosporins
- have a B-lactam ring - different structures (extra carbon) makes them more resistant to B-lactamases than penicillins - group R1 and R2 can be substituted to produce a variety of cephalosporins
65
see slide 34: generations of cephalosporins
see slide 34: generations of cephalosporins
66
MAO of cephalosporins
-inhibit cell wall synthesis by inhibiting transpeptidase, this blocking cross-link of peptidoglycan
67
see charts
see charts

Pharmacology (23 decks)

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