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pharmacology > intro to Abx,Cell wall/membrane attackers > Flashcards

intro to Abx,Cell wall/membrane attackers Flashcards

1
Q

bactericidal

A 
DNA replication (fluroQ + metronizadole) 
RNA replication (rifampin) 
cell wall attackers (except beta lactamase) 
cell membrane (polymixins, daptomycin)
proteins: ONLY macrolides, streptoGs,aminoGs
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2
Q

batcteriostatic

A 
"ECSTaTiCO about bacteriostatic" to be alive :)
Erythromycin
Clindamycin
Sulfonamides
Trimethoprim
Tetracyclines 
Oxazolianones (linezolid)
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3
Q

combination therapy:syngery

A

increase killing power:
Utilize this when organism is unknown or special indications such as infectious endocarditis or tuberculosis

Concerns for combination therapy include:
Development of resistance
One drug interfering with the action of another
Tetracycline (bacteriostatic) interfering with penicillins (bactericidal)

ex/ PCN (cell wall) and aminoglycoside (protein synthesis): can get into cell wall to target ribosome.

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4
Q

combination therapy: antagonism

A

dont combine bactericidal and bacteriostatic- can use 2 Cidals or 2 Statics (slow growth inhibits cidal)

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5
Q

PCN: MOA, Adverse effects

A

MOA: crosslinking of cell wall (peptidoglycan)
Adverse: NEPHRITIS, hematologic (bleeding and clotting), NEUROTOXICITY, secondary infections, hypersensitivity

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6
Q

PCN: spectrum, clinical uses

A

spectrum: Gram + (cocci, rods, anerobes), Gram - (cocci), spirochete.
uses: syphilis, gangrene

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7
Q

PCN: 3 types and spectrum differences

A

natural
antistaph (B Lactamase resistant): add MSSA, Streptococcus A and B
extended spectrum: Add gram - (can get through outer membrane) .
–>Amp/Amox: add + and -, subtract MSSA
–>Piper/Tic: add + (including pseudomonas, Klebsiella, Enterobacter)

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8
Q

PCN- natural group

A

“Natural Voluptous Girls Benza-yonce”

G, V, Benzathine

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9
Q

PCN- AntiStaph

A 
"you take drug test for staff?" - "Nah im chillin, Oxy and Meth Dictate" 
Naficillin
Oxacillin
Methacillin
Dicloxacillin
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10
Q

PCN- extended spectrum

A

Ampicillin/Amoxicillin

Pipercillin/Ticarcillin

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11
Q

Abx that attack cell wall synthesis

A

Beta Lactams (PCNs, Cephalosporins, Monobactams, Carbopenems)
–>Beta Lactamas inhibitors (“CAST”: Clavulanic Acid,
Avibactam, Sulfabactam, Tazobactam)

Glycopeptides
Bacitracin
Fosfomycin
cycloserine (not as important)

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12
Q

Abx that attack protein synthesis

A

50s subunit: Macrolides, Clindamycin, Streptogramins, Oxazolidones
30s Subunit: Tetracyclines, Aminoglycosides

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13
Q

Abx that attack cell membrane integrity

A

Polymixins

Daptomycin

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14
Q

Abx that attack metabolic pathways (folate synthesis)or action

A

sulfanomide, trimethoprim

(PABA- folate- purines)

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15
Q

Abx that attack Nucleic acid synthesis

A

fluoroquinolones and metronizadole - DNA

Rifampin- RNA

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16
Q

only place in the body where you shouldnt have normal flora

A

lungs

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17
Q

common offenders with no cell wall (aka can’t use cell wall attacker)

A

TB, mycoplasm pneumoniae, chlamydia pneumoniae, legionella pneumoniae

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18
Q

difficult areas to determine if normal flora is a problem

A

sputum, urine from women (dirtier areas)

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19
Q

empiric treatment

A

Selecting an agent to treat an ill patient based on presumed infection (signs and symptoms). dont wanna wait for C&S- either critically ill pt, immunosuppressed, easy to identify
=treat with broad spectrum right away, then maybe do C&S

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20
Q

min. inhibitory conc. vs. min bactericidal conc.

A

Minimum Inhibitory Concentration
Lowest antimicrobial concentration that prevents growth of an organism 24 hours after administration

Minimum Bactericidal Concentration
Lowest antimicrobial concentration that kills 99.9% of bacteria
minimum inhibitory conc- goes along with bacteriostatic - can use these at lower agents and increase it to become bactericidal

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21
Q

factors that affect effective conc of drug

A

Impacted by:
Capillaries ability to carry drug to tissue site

Natural barriers: CNS, placenta, vitreous body of eye

Blood Brain Barrier (BBB)- very tight junctions
For agent to cross BBB is must possess the following:
High lipid solubility
Low molecular weight
Low protein binding

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22
Q

reasons to give drugs parenterally

A

-For increased bioavailability
Drug is avoiding first pass metabolism by liver
-Need increased absorption due to gut malabsorption issue
-Necessary for high concentrations (meningitis & endocarditis)
-Also give IV or IM if can’t take oral medications
Vomiting or drug not absorbed orally

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23
Q

when can you change IV or oral medication?

A

General rule: when seeing signs of improvement, fever down and focal symptoms better, and have an equivalent oral antibiotic then switch to it
A popular time to do this is once culture results back (48 hours) as culture will help tell you which oral antibiotic will be effective

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24
Q

conc dependent killing, time dependent killing, postantibiotic effect

A

-Concentration-dependent killing
Once daily dosing to achieve high peak levels
Leads to rapid killing of pathogen
Ex. Aminoglycosides, fluoroquinolones

-Time-dependent (concentration-independent) killing
Multiple doses or continuous IV infusion
Increased efficacy of antimicrobial when the blood conc. remain above MIC (min inhib conc.) for extended periods of time to kill more bacteria
Beta-lactams, macrolides

-Postantibiotic effect
Persistent suppression of microbial growth after antibiotic levels fall below MIC.
Ex. Aminoglycosides, fluoroquinolones

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25
Q

mechanisms of resistance to antibiotics (by bacteria)

(4 main)

A 
Destruction or Inactivation of Drug
Mutation of Target Site
Efflux of Drug
Genetic Transfer
-Conjugation
-Transformation
-Transduction
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26
Q

common contributors to hypersensitivity (drug allergy)

A

beta lactams and sulfas

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27
Q

3 complications of antibiotics therapy

A

hypersensitivity, toxicity (adverse effect), superinfection

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28
Q

B lactamase inhibitors: function

A

Beta lactamases:source of resistance.
used in combo with abx
inhibit the enzyme produced by the bacteria (w/abx)= bacteria will not be as resistant to the antibiotic.

Available in fixed combinations (ex. amox/clav=augmentin)
The dose is based on the strength of the primary antibiotic – not the beta lactamase inhibitor.

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29
Q

Beta Lactamase inhibitors

A 
"CAST"
Clavulanic Acid 
Avibactram (w/ ceftazidime) 
Sulfabactam
Taxobactam
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30
Q

cephalosporin generation categorizing

A

Five generations based on when they are made & what they kill.

When a significant modification was made to the group that really changed the spectrum it was called a new generation.

First generation the oldest
Currently on fifth generation

31
Q

ceph 1st gen and their spectrum

A 
cefazolim + cephalexin 
gram + cocci (strep and staph)
"PEcK"
Proteus mirabilis
E. Coli
Klebsiella
32
Q

which cephalosporin is secreted by bile/feces?

A

ceftriaxone- so no dosage adjustment needed for renal/hepatic comprimised individuals

33
Q

admin and distribution of cephalosporins

A

Administration: Many IV, fewer oral-poor oral absorption
Distribution: Good, but CSF penetration limited to
Ceftriazone, cefotaxime
All cross placenta

34
Q

adverse effects of cephalosporins

A
  1. super infections
  2. low prothrombin
  3. disulfuram-like effect
  4. increase nephrotoxicity risk with aminoglycosides
35
Q

common superinfections/secondary infections

A

Cdiff, Vaginal candidas, thrush

*all can occur with cephalosporins

36
Q

klebsiella can cause what?

A

Klebsiella: Gram-negative

pneumonia, blood infections, wound or surgical site infections, meningitis, etc

37
Q

cephalexin used for what?

A

UTIs, Skin infections, otitis media, pharyngitis

38
Q

2nd gen cephalosporins

A 
Cefaclor 
Cefoxitin
Cefuroxime 
Cefprozil 
Cefotetan

“Fake Fox Fur ( is) Proper To Tan”

39
Q

ceforoxime is good to use for what?

A

CAP (community acquired pneumonia- kills Hflu and strep pneumonia

40
Q

2nd gen cephalosporin spectrum

A 
PEcK.. add "HENS"
H. Flu
Enterobacter
Neisseria
Serratia mercescens

*good for lower respiratory infections

41
Q

3rd gen cephalosporins

A 
Cefdinir 
Ceftriaxone 
Ceftazidime 
Cefotaxime 
Cefpodoxime

“Dine Alone” all end in “ime”
*exceptions, cefepime (4th gen), ceforoxime (2nd gen)

“Ceftaz as tazmanian devil- potent and only one that gets pseudamonas)

42
Q

what do we use to treat gonorrhea?

A

3rd gen cephalosporins

…” cause once you have gonorrhea, you Dine Alone”

43
Q

4th gen cephalosporins

A

cefepime - think “prime”-alone

spectrum: add- stronger against pseudomonas
- more resistant to beta lactamases

44
Q

treatment for meningitis

A

ceftriaxone or cefotaxime b/c can get into CNS

3rd gen cephalosporins

45
Q

5th gen cephalosporin and spectrum

A 
ceftaroline 
Broad spectrum
Add: gram + and -
"LAME"
Listeria
Atypical (chlamydia, mycoplasma)
MRSA
Enterococci faecalis

SUBTRACT: pseudomonas

46
Q

monobactams: abx w/in, MOA, spectrum

A

Aztreonam
MOA: cell wall synthesis (less susceptible to beta lactamases than PCN)
Spectrum:
Great Gram neg. aerobic rods & Pseudomonas aeruginosa
Hospital drug for serious gm – infections that are resistant to other drugs or if penicillin allergic and can’t use other drugs

47
Q

carbapenems

A 
"DIME" 
Doripenem
Imipenem
Meropenem
Ertapenem
48
Q

carbapenems: MOA and Spectrum

A

MOA: cell wall
Spectrum: BROADEST of all beta lactams
gram +, -, anerobes
for life threatening infections

49
Q

what is the broadest spectrum of beta lactams?

A

carbapenems the “DIME” of the dozen

50
Q

carbapenems: adverse effects

A

CNS toxicity (risk for seizure) @ high plasma conc.- highest in meropenem

51
Q

renal excretion of PCN is inhibited by what drug?

A

probenecid

52
Q

Vancomycin is used to treat what major infections?

A

Cdiff, MRSA, Enterococci

53
Q

bacitracin is used primarily for what?

A

topically for infections caused by gram + cocci

54
Q

fosfomycin is used for what?

A

uncomplicated UTIs (from Ecoli or enterococci)

55
Q

Abx that attack cell wall but have no B Lactam ring

A

glycopeptides, bacitracin, fosfomycin

cycloserine, not in slideshow

56
Q

Vancomycin: what group?

MOA, bactericidal?, spectrum

A 
glycopeptide
cell wall- D-ALA-D-ALA (growing peptide) = inhibition of transpepsidase- preventing crosslinking
Bactericidal: yes- time-dependent
Spectrum:
gram + (MRSA, enterococcus, Cdiff)
57
Q

vancomycin PK

A

Not absorbed from GI tract, given IV
If given orally it is not being absorbed and giving it to act topically in the GI tract (C. diff)
Slow administration – 1 hour
*significant renal excretion

58
Q

vancomycin: adverse rxns

A

“Well tolerated but NOT trouble free”
-Nephrotoxicity – especially if given with other nephrotoxic drugs (aminoglycosides)
-Ototoxicity - especially if given with other ototoxic drugs (aminoglycosides)
-Thrombophlebitis
Irritates tissue at site of injection

And-redman’s syndrome
skin flushing low BP from histamine release when give IV too fast

59
Q

cell membrane attacking abx

A

daptomycin, polymixin B and E

60
Q

Daptomycin: bactericidal? Spectrum? clinical uses?

adverse effects?

A

yes- conc. dependent
MRSA, enterococcus (including VRE)

uses:
sepsis, endocarditis, complicated skin and soft tissue infections

toxicity: skeletal muscle- myalgia and weakness

61
Q

polymixin B and E: MOA, bactericidal, spectrum

A

MOA: cell membrane

bactericidal: YES, time-dependent
spectrum: gram neg. (pseudomonas, E. Coli, Klebsiella)

62
Q

polymixin B and E: adverse effects

A

nephrotoxicity and neurotoxicity

63
Q

fosfomycin: MOA, bactericidal

A

“cell membrane” category - targets early cell wall synthesis

bactericidal: YES

64
Q

fosfomycin: spectrum and uses

A

spectrum: Gram + and - in urine only
uses: uncomplex UTI only

65
Q

two Abx ecreted via biliary

A

ceftriaxone and nafcillin

66
Q

treatment for pharyngitis?

A

PCN V - bacteria is form of streptococci

67
Q

PCN will generally treat what?

aminoglycoside will generally treat what?

A

PCN: gram + (streptococci, staphylococci), syphilis, gangrene
AmG: gram - (pseudomonas, enterobacter)

68
Q

cephalexin generally used to treat what?

A

skin and soft tissue infections

69
Q

nafcillin, oxacillin generally treat what?

A

staph aureus (osteomyelitis, endocarditis, etc)

70
Q

cefazolin generally used for what?

A

perioperative prophylaxis (staphylococci, Ecoli)

71
Q

ceftotetan generally used to treat what?

A

intra-ab, gyn, biliary infections (aerobic and anaerobic bacilli)

72
Q

cefdinir, cefprozil, ceforoxime generally used to treat what?

A

respiratory tract, skin and soft tissue infections (pneumococci, H Flu)

73
Q

ceftriaxone generally treats what?

A

gonorrhea (gonococci), UTI, meningitis (meningococci)

74
Q

go to treatment for endocarditis?

A

amoxicillin

pharmacology (24 decks)

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