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Cell Wall Inhibitors Flashcards

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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
MoA of cephalosporins
inhibit transpeptidase PBP1a, 1b, PBP3
26
Ceftobiprole Medocarila
broad spectrum cephalosporin derivative high affinity for PBP2a for MRSA and PBP2x for resistant strep. knocks everything down
27
T1/2 for 1st gen & 4th gen cephalosporins
1-2 hours | 4th gen readily penetrate the CNS
28
T1/2 for 2nd gen & 3rd gen cephalosporins
wide range: 1-8hr
29
AE for cephalosporins:
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
Special considerations for cephalosporins
MTT (methytetrathiazole) increased effects of warfarin. alcohol intolerance because acetaldehyde dehydrogenase increased nephrotoxicity with ahminoglycosides probenecid (gout) increase plasma levels milk protein hypersensitivity
31
B-lactamase inhibitors
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
MoA of B-lactamase inhibitors
covalently bonds with B-lactamases to make table intermediates - > prevents interactions with penicillins
33
Excretion of B-lactamase inhibitors
``` 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
names some Carbapenems
Imipenem-cilistatin Meropenem Ertapenem Doripenem
35
Carbapenem spectrum
broad spectrum - g(-) and g(+) aerobic and anaerobic better than pen G = better g(+) not active against MRSA or C.difficile
36
Use of carbapenem
moderate to severe nosocomial and polymicrobial infections = imipenem, meropenem, doripenem mild to moderate community acquired infections = ertapenem **NOT FOR NOSOCOMIAL**
37
MoA of carbapenems
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
Absorption/excretion of Carbapenems
Parenterally - poor stability in GI and poor absorption Short half life (1hr) most excreted unchanged in glomerular filtration
39
How is imipenem excreted?
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
AE of carbapenems
blood and clotting problems with imipenem seizures with imipenem okay for pregnancy
41
special considerations with carbapenems
- 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
Monobactam spectrum
Gram negative aerobic bacteria that are resistant to B-lactamases **DOES NOT WORK WITH G(+) anaerobic**
43
Clinical use of monobactams
Used as Azetreonam. UTI's, lower respiratory infections, skin... patients with severe allergy to penicillins and cephalosporins
44
MoA of monobactams
binds to and inhibits PBP3 in g(-) bacteria | changes cell shape structure so that it no longer works`
45
Absorption/elimination of monobactams
not absorbed by GI tract glomerular filtration elimination adjusted to renal failure
46
AE of monobactams
Elevated liver enzymes
47
Special considerations for monobactams
B-lactamase inducing abx may increase resistance to Aztreonam
48
Vancomycin spectrum
G(+) aerobic or anaerobic | not effective against Listeria (which is G+)
49
Clinical uses of vancomycin
prophylaxis: surgical implant, MSSA or MRSA in hemodialysis, respiratory/GI/ Genitourinary procedures C. difficile Staph. enterocolitis
50
MoA of vancomycin
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
Absorption/ elimination of vancomycin
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
AE of vancomycin
nephrotoxicity | RED MAN SYNDROME (immediate reaction: severe hypotension and cardiac arrest due to fast IV infusion)
53
special considerations for vancomycin
increased risk or nephrotoxicity with ahminoglycosides, bacitracin, polymixin B. flushing with anesthetics neuromuscular blockade increase with muscular relaxants
54
Telavancins are...
semi-synthetic analog of vancomycin
55
Telavancin spectrum
G(+). effective against MSSA and MRSA. more potent than vancomycin for decreasing biofilm formation. effective for E. faecium and faecalis
56
Clinical use of Telavancin
skin and skin structure infections by susceptible strains. | Nosocomial pneumonia
57
MoA of Telavacin
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
Excretion of Telavacin
LONG half life (9hrs) normal renal function excreted in urine high plasma protein binding
59
AE of Telavacin
taste disturbance, | increase serum creatinine, low K
60
Daptomycin spectrum
aerobic and anaerobic G(+). | effective against stop (MSSA/MRSA) and strep A, D
61
Clinical use of Daptomycin
same as Telavancin: skin and skin structure infections. Nosocomial pneumonia
62
MoA of Daptomycin
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
Daptomycin Elmination
Long half life (8-9 hours) & PAE (5-10hr) | unchanged in urine. clearance decreased in obese pts (highly lipid)
64
AE of daptomycin
Regular: NVD, injection site, headache, fever, | INSOMINIA
65
special considerations of daptomycin
interactions with HMG-CoA reductase inhibitors (statins): increases risk for myopathy. dose change for hemodialysis
66
Polymyxins examples
Polymyxin B - parenteral Colistin (topical and oral) Colistimethate (oral)
67
spectrum of polymyxins
G(-) esp. for p. aeruginosa | NOT FOR g(-) or g(+) aerobic cocci or g(+) aerobic bacilli
68
Clinical use for polymyxins
when nothing else works
69
MoA of polymyxins
binds to and neutralizes LPS (inflammation). reacts with lipid A (part of LPS) to make pore-like structures to disrupt membrane.
70
Elimination of polymyxins
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
AE of polymyxins
``` Nephrotoxicity (reversible) tubular necrosis (acute) neuromuscular blockade (like daptomycin and vancomycin) ```

Drugs And Infectious Diseases (4 decks)

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