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Drugs And Infectious Diseases > Cell Wall Inhibitors > Flashcards

Cell Wall Inhibitors Flashcards

1
Q

Penicillin G & V spectrum

A

Gram (+) microbes have the greatest activity
gram (-) cocci -> not as good because need to get through cell wall where B-lactamase is waiting
and non-B-lactamase producing anaerobes
Susceptible to B-lactamase activity

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2
Q

B-lactamase resistant penicillins spectrum

A

Nafcillin, Dicloxacilliin
Against Strep, staph, pneunmococci
No activity against enterococci and anaerobes or gram (-) rods or cocci

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3
Q

Aminopenicillins and extended spectrum penicillins

A

amoxicillin, ampicillin
similar to penicillin in spectrum
BUT WITH GREATER ACTIVITY AGAINST GRAM (-)
often with B-lactamase inhibitors like clavulanic acid (increases the activity of the abx)

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4
Q

Indication and drug of choice for Penicillin G

A

Streptococci, Meningococci, PEN- susceptible pneumococci

for Antrax, diptheria, C. difficile, syphillis, meningitis

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5
Q

Indication and drug of choice for Penicillin V

A

Poor availability -> mild infections
Step. A,C,G (pharyngitis and tonsilitis)
PEN -sensitive S. pneumonaie

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6
Q

Clinical uses for Nafcillin and Dicloxacillin - B-lactamase resistant

A

Penicillnase producing staph,
MSSA - methicillin susceptible s. aureus
prosthetic valve infection

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7
Q

Aminopenicillins - ampicillin and amoxicillin

A

drug of choice for pneumococci
shigella and other GI infections
Gonorrhea
Respiratory infections

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8
Q

Ticarcillin, Piperacillin, Azlocillin - extended spectrum

A 
drug of choice for pseudomonas
also for shigella and other GI
bone and joint infections
skin infections
also used for lower respiratory and UTI where access is difficult
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9
Q

MoA of penicillins and cephalosporins

A

Inhibit transpeptidase PBP1a and PBP1b -> prevents D-ala removal on the 5th position

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10
Q

Absorption of Pen G

A

IV or IM because unstable in gastric acid - destroyed

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11
Q

Absorption of Nafcillin, ticarcillin, piperacillin

A

IV or IM because poor GI absorption

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12
Q

Pen V, Dicloxacillin, Ampicillin: special consideration when administered

A

can be given orally but food interferes with absorption

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13
Q

Elimination of Penicillin drugs

A 
All unchanged in the urine
Rapid elimination (30mins- 1.5hr)
All except for amoxicillin have some biliary excretion
Ticarcillin and piperacillin: biliary excretion is increased with renal deficiency
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14
Q

AE for penicillin drugs

A

Common:
NVD (increased risk with amoxicillin), Allergic reactions, phlebitis- inflammation of veins (Ticarcillin and piperacilin)
Rare:
neutropenia (pen G, nafcillin, piperacillin)
CNS effects (confusion, seizures)
Hyperkalemia (pen G K+)
dizziness, tinnitus, headache (Pen G procaine)

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15
Q

Special considerations for Penicillins

A

Increased risk of rash with amoxicillin with allopurinol
Pen G and V decrease effectiveness of birth control pills
Colestipol (cholesterol) decrease Pen V absorption
Probenecid (gout) increases plasma levels with pen G and V

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16
Q

Cephalosporins First generation

A 
very active against gram (+) aerobic cocci
Pen-sensitive staph and strep
NOT active against enterococci
little g(-)
Cefazolin
Cephalexin
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17
Q

Cephalosporins Second generation

A 
active against g(+) aerobic cocci but not as much as 1st gen
but has better g(-)
mouth but not GI anaerobes 
Loracarbef
Cefonicid
cefaclor
cefuroxime
cefprozil
cefazolin (parenteral)
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18
Q

3rd generation cephalosporin

A 
inferior to 2nd and 1st for g(+) 
good against g(-)
broad coverage of enterobacteria
NO GI anaerobes
cefixime
cefotaxime
Cefoperaxone (doesn't go to CNS & biliary excretion)
Ceftriaxone (biliary excretion- reversible obstructive toxicity)
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19
Q

4th generation cephalosporin

A

less potent than 1st gen but more than 3rd gen against g(+) EXCELLENT against g(-)
better than 3rd gen!
cefeprime

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20
Q

Cephamycins

A

Cefoxitin
not “true” 2nd generation
less active against G(+) cocci
CAN GO AGAINST SOME ENTEROBACTERIA
Used: anaerobic/aerobic infections of the skin/ soft tissue
intra-abdominal or gynecological surgical prophylaxis

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21
Q

Clinical use of first generation cephalosporin

A

uncomplicated, community acquired skin and soft tissue infections and UTI
respiratory infection by PEN sensitive bacteria
surgical wound prophylaxis (parenteral)

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22
Q

Clinical use of 2nd generation cephalosporin

A

community acquired respiratory infection

uncomplicated UTI by E.coli

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23
Q

clinical use of 3rd generation cephalosporin

A

hospital acquired gram (-) infections
all kinds of complicated community acquired infections
lyme disease, severe shigella, typhoid fever

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24
Q

clinical use of 4th gen cephalosporin

A

moderate to sever nosocomial acquired infections
uncomplicated and complicated UTI, skin and soft tissue infections
Pneumonia bacteremia

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25
Q

MoA of cephalosporins

A

inhibit transpeptidase PBP1a, 1b, PBP3

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26
Q

Ceftobiprole Medocarila

A

broad spectrum cephalosporin derivative
high affinity for PBP2a for MRSA and PBP2x for resistant strep.
knocks everything down

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27
Q

T1/2 for 1st gen & 4th gen cephalosporins

A

1-2 hours

4th gen readily penetrate the CNS

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28
Q

T1/2 for 2nd gen & 3rd gen cephalosporins

A

wide range: 1-8hr

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29
Q

AE for cephalosporins:

A

Common: NVD, allergic rxns
ceftrioxone - reversible obstructive excretion
Rare: blood cell problems, granulocytopenia (bone marrow suppression), renal tubular necrosis (most are excreted through the kidneys)

30
Q

Special considerations for cephalosporins

A

MTT (methytetrathiazole) increased effects of warfarin.
alcohol intolerance because acetaldehyde dehydrogenase
increased nephrotoxicity with ahminoglycosides
probenecid (gout) increase plasma levels
milk protein hypersensitivity

31
Q

B-lactamase inhibitors

A

not used separated because have weak abx activity- potent inhibitors of B-lactamases
Drugs:
Clavulinic acid
Sulbactam
Tazobactam
Restore the abx properties of aminopenicillins, piperacillin and ticarcillin.

32
Q

MoA of B-lactamase inhibitors

A

covalently bonds with B-lactamases to make table intermediates - > prevents interactions with penicillins

33
Q

Excretion of B-lactamase inhibitors

A 
they are all excreted in urine 
Clavulinic acid also secreted as metabolites in lungs and feces
sulbactam minor biliary excretion
low CNS penetration
absorbed in GI tract
34
Q

names some Carbapenems

A

Imipenem-cilistatin
Meropenem
Ertapenem
Doripenem

35
Q

Carbapenem spectrum

A

broad spectrum - g(-) and g(+) aerobic and anaerobic
better than pen G = better g(+)
not active against MRSA or C.difficile

36
Q

Use of carbapenem

A

moderate to severe nosocomial and polymicrobial infections = imipenem, meropenem, doripenem
mild to moderate community acquired infections = ertapenem NOT FOR NOSOCOMIAL

37
Q

MoA of carbapenems

A

inhibit PBP activity
affinities for Imipenem: PBP2»PBP1a»PBP3a
Meropenem, Ertapenem: PBP2, PBP3>PBP1a, 1b
Doripenem: high affinity for PBP1a, 1b, PBP2, 3, 4
NO affinity for PBP2a (MRSA) or PBP2x (resistant strep)

38
Q

Absorption/excretion of Carbapenems

A

Parenterally - poor stability in GI and poor absorption
Short half life (1hr)
most excreted unchanged in glomerular filtration

39
Q

How is imipenem excreted?

A

It is hydrolyzed at the brush borders of renal tubules by dehydropeptidase.

  • *must be given with cilistatin (DHPI inhibitor) or else metabolites are NEPHROTOXIC
  • also enhances the ability of imipenem
40
Q

AE of carbapenems

A

blood and clotting problems with imipenem
seizures with imipenem
okay for pregnancy

41
Q

special considerations with carbapenems

A
  • cross reactive with other B-lactam abx
  • any drug cause causes decrease in glomerular filtration
  • increased risk of seizures with imipenem and ganciclovir
  • Probenecid increases serum levels with meropenem
  • Ertapenem diluted with lidocaine is contraindicated in pots with hypersensitivity to amide local anesthetics
42
Q

Monobactam spectrum

A

Gram negative aerobic bacteria that are resistant to B-lactamases
DOES NOT WORK WITH G(+) anaerobic

43
Q

Clinical use of monobactams

A

Used as Azetreonam.
UTI’s, lower respiratory infections, skin…
patients with severe allergy to penicillins and cephalosporins

44
Q

MoA of monobactams

A

binds to and inhibits PBP3 in g(-) bacteria

changes cell shape structure so that it no longer works`

45
Q

Absorption/elimination of monobactams

A

not absorbed by GI tract
glomerular filtration elimination
adjusted to renal failure

46
Q

AE of monobactams

A

Elevated liver enzymes

47
Q

Special considerations for monobactams

A

B-lactamase inducing abx may increase resistance to Aztreonam

48
Q

Vancomycin spectrum

A

G(+) aerobic or anaerobic

not effective against Listeria (which is G+)

49
Q

Clinical uses of vancomycin

A

prophylaxis: surgical implant, MSSA or MRSA in hemodialysis, respiratory/GI/ Genitourinary procedures
C. difficile
Staph. enterocolitis

50
Q

MoA of vancomycin

A

Binds with high affinity to D-ala, D-ala terminus
DOES NOT interact with PBPps
prevents interaction with transglycosylase blocking growth of peptidoglycan chain

51
Q

Absorption/ elimination of vancomycin

A

poor oral absorption ->IV
readily goes into CSF
excreted unchanged in urine -> depends on CrCl
Long half life (6h) with 2-4x MIC, PAE last 2-7hr
watch the CrCl

52
Q

AE of vancomycin

A

nephrotoxicity

RED MAN SYNDROME (immediate reaction: severe hypotension and cardiac arrest due to fast IV infusion)

53
Q

special considerations for vancomycin

A

increased risk or nephrotoxicity with ahminoglycosides, bacitracin, polymixin B.
flushing with anesthetics
neuromuscular blockade increase with muscular relaxants

54
Q

Telavancins are…

A

semi-synthetic analog of vancomycin

55
Q

Telavancin spectrum

A

G(+). effective against MSSA and MRSA.
more potent than vancomycin for decreasing biofilm formation.
effective for E. faecium and faecalis

56
Q

Clinical use of Telavancin

A

skin and skin structure infections by susceptible strains.

Nosocomial pneumonia

57
Q

MoA of Telavacin

A

1) same as vancomycin: binds to D-ala, D-ala terminus to stop inhibiting peptidoglycan chains
2) Lipid side chain acts as a detergent to destroy membrane

58
Q

Excretion of Telavacin

A

LONG half life (9hrs) normal renal function
excreted in urine
high plasma protein binding

59
Q

AE of Telavacin

A

taste disturbance,

increase serum creatinine, low K

60
Q

Daptomycin spectrum

A

aerobic and anaerobic G(+).

effective against stop (MSSA/MRSA) and strep A, D

61
Q

Clinical use of Daptomycin

A

same as Telavancin:
skin and skin structure infections.
Nosocomial pneumonia

62
Q

MoA of Daptomycin

A

Concentration dependent - Ca++
Daptomycin inserted into the lipid bilayer (creates a channel) and then depolarizes the membrane with K+ efflux resulting in rapid cell death

63
Q

Daptomycin Elmination

A

Long half life (8-9 hours) & PAE (5-10hr)

unchanged in urine. clearance decreased in obese pts (highly lipid)

64
Q

AE of daptomycin

A

Regular: NVD, injection site, headache, fever,

INSOMINIA

65
Q

special considerations of daptomycin

A

interactions with HMG-CoA reductase inhibitors (statins): increases risk for myopathy.
dose change for hemodialysis

66
Q

Polymyxins examples

A

Polymyxin B - parenteral
Colistin (topical and oral)
Colistimethate (oral)

67
Q

spectrum of polymyxins

A

G(-) esp. for p. aeruginosa

NOT FOR g(-) or g(+) aerobic cocci or g(+) aerobic bacilli

68
Q

Clinical use for polymyxins

A

when nothing else works

69
Q

MoA of polymyxins

A

binds to and neutralizes LPS (inflammation). reacts with lipid A (part of LPS) to make pore-like structures to disrupt membrane.

70
Q

Elimination of polymyxins

A

highly bound to membrane lipids in many tissues-> slow release of drug from bound tissue
half like moderate (3.5-6h)
unchanged in urine

71
Q

AE of polymyxins

A 
Nephrotoxicity (reversible)
tubular necrosis (acute)
neuromuscular blockade (like daptomycin and vancomycin)

Drugs And Infectious Diseases (4 decks)

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