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Pharmacology > Antibiotics > Flashcards

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
Q

what type of bacteria is Pseudomonas aeruginosa

A

gram-(-), aerobic

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26
Q

pseudomonas aerguinosa is a major cause of

A

hospital infections

-prevalent among patients with burn wounds, acute leukemia, IV drug additions

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27
Q

what type of bacteria is Vancomycin-Resistant Enterococci

A

gram-(-) anaerobic

28
Q

what type of bacteria is Clostridium

A

gram- (+), anaerobic, produces destructive exotoxins

29
Q

what type of baxter is enterobacteriaceae

A

gram-(-), anaerobic, can cause fatal abscesses and bacteremias

30
Q

what are the bacteria cell wall synthesis inhibitors

A
  1. penicillins “-cillin”
  2. cephalosporins “cef~1-4th gen”
  3. carbapenems and monobactam
  4. others: vancomycin, bacitracin, fosfomycin & cycloserine
31
Q

mechanism of bacteria cell wall synthesis inhibitors

A

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
Q

what are the B-lactam antibiotics

A

penicillins:

  • penicillin G
  • penicillin V
  • Oxacillin
  • Dicloxacillin
  • Ampicillin
  • Amoxicillin
  • Ticarcillin
  • Mezlocillin
33
Q

what is the structure of penicillin

A
  • 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
Q

what is penicillin G

A
  • the only natural penicillin

- used in the form of benzathine, procaine, potassium & sodium salts

35
Q

what is penicillin V

A

semi-synthetic

36
Q

what are the narrow spectrum penicillins

A
  • oxacillin

- dicloxacillin

37
Q

what are the broad-spectum pencillins

A
  • ampicillin (amino pencillins)
  • amoxicillin (amino penicillin)
  • ticarcillin (carboxy penicillins)
  • mezlocillin (acylureido penicillins)
38
Q

define bactericidial

A

kill bacteria

39
Q

define bacteriostatic

A

inhibit microbial growth

40
Q

define beta-lactam antibiotics

A

drugs with structures containing a beta-lactam ring

41
Q

what is MIC

A

lowest concentration of antimicrobial drug capable of inhibiting growth of an organism

42
Q

what is penicillin-binding proteins (PBPS)

A

bacterial cytoplasmatic membrane proteins that act as the initial receptors for penicillins and other beta-lactam antibiotics

43
Q

what is peptidoglycan

A

chains of polysaccharides and peptides polypeptides that are cross-linked to form the bacteria cell wall

44
Q

what is selective toxicity

A

more toxicity to the invader than to the host

45
Q

what is transpeptidases

A

bacterial enzymes involved in the cross-linking of linear peptidoglycan chains, the final step in cell wall synthesis

46
Q

penicillins and cephalosporins are the major antibiotics that inhibit

A
  • bacterial cell wall synthesis

- inhibit the synthesis of peptidoglycan (PG) by inhibiting transpeptidase (transpeptidation)

47
Q

what are the antimicrobials are narrow spectrum

A

-natural penicillin (G)
-semisynthetic penicillin V
-anti-staphylococcal pencillins:
Isoazolyl penicillins:
Oxacillin
Dicloxacillin

48
Q

what are the antimicrobials that are broad spectrum

A 
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
Q

what are the clinical uses of antimicrobials

A
  1. septicicemia
  2. meningitis
  3. hospital-acquired (bacterial) penumonia
  4. cellulitis
  5. bone and joint infections
  6. acute/chronic urinary tract infections
50
Q

how does resistance to antimicrobials occur

A
  1. inactivation by bacterial B-lactamases
  2. mutant transpeptidases
  3. down-regulation of porins
  4. efflux pump
51
Q

inactivation by bacterial B-lactmase is most common in what bacteria

A

Staphylococcus aureus
Pseudomonas aeruginosa
E.coli
enterobacters

52
Q

what is mutant transpeptidases

A

alterations in the drug targeted Penicillin binding proteins, reduce the affinity for drug binding in staphylococci, pneumococci and enterococci

53
Q

effects of down-regulation of porins

A

impairs drug penetration via porins in gram-(-) bacteria

54
Q

pharmacokinetics of antimicrobials

A

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
Q

what are the adverse rxns of antimicrobials

A
  • 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
Q

what are the drug interactions with penicillin

A

-very few; in vitro mixing with aminoglycosides reduces the activity of both

57
Q

what is probenecid

A

an uricosuric agent which increases excretion of uric acid in hyperuricemia, decreases excretion of penicillins

58
Q

describe the structure of B-lactamase inhibitors

A
  • 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
Q

see slide 31

A

see slide 31

60
Q

what is septicemia

A

commubity and hospital-acquired pneumonia, cellulitis, sinusitis, bone and joint infection

61
Q

how is clavulanate absorbed

A

after oral administration

62
Q

how is sulbactum & tazobactum administered

A

IV due to poor oral administration

63
Q

piperacillin increases the half life of

A

tazobactum

64
Q

describe the structure of cephalosporins

A
  • 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
Q

see slide 34: generations of cephalosporins

A

see slide 34: generations of cephalosporins

66
Q

MAO of cephalosporins

A

-inhibit cell wall synthesis by inhibiting transpeptidase, this blocking cross-link of peptidoglycan

67
Q

see charts

A

see charts

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