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PHRM 865 > Exam 2 - Cushman/Erdman (Drug Classes) > Flashcards

Exam 2 - Cushman/Erdman (Drug Classes) Flashcards

1
Q

Beta Lactam Characteristics: “The 6 things”

They all have the same MOA — what is it?

A

inhibit cell wall synthesis

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2
Q

Beta Lactam Characteristics: “The 6 things”

They all have the same MORs — what are they

A

beta lactamase degradation, PBP alteration, decrease penetration

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3
Q 
Beta Lactam Characteristics: "The 6 things"
They are (bactericidal or bacteriostatic) in a (time or concentration) dependent matter

*one exception is ___________

A

bacteriocidal; time dependent

exception: they are NOT bacteriocidal to enterococcus (they are only bacteriostatic to it)

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4
Q

Beta Lactam Characteristics: “The 6 things”

They have a (short or long) half life?

A

short!! (< 2 hours!!!)

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5
Q

Beta Lactam Characteristics: “The 6 things”
They are primarily excreted _________
The exceptions are what?

A

excreted renally mainly

exceptions are Nafcillin, Oxacillin, Ceftriaxone, and Cefoperazone

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6
Q

Beta Lactam Characteristics: “The 6 things”

All have Cross-allergenicity (except _______)

A

aztreonam

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7
Q

what are the 4 main groups of beta lactam abx

A

Penicillins
Cephalosporins
Carbapenems
Monobactams

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8
Q

PCNs:

inhibit PBPs and thus inhibit the final ________ step of ________ synthesis

A

final transpeptidation step

peptidoglycan synthesis

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9
Q

What are common bugs that are resistant to penicillins due to alteration in structure of PBPs?

A

MRSA (methicillin resistant staphylococcus aureus)
and
PRSP (penicillin resistant streptococcus pneumoniae)

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10
Q

What drugs are the natural penicillins

A

Aqueous Pencillin G
Benzathine Penicillin G
Procaine Penicillin G
Phenoxymethyl Penicillin (aka Penicllin VK)

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11
Q

what drugs are the Penicillinase Resistant Penicillins

A 
Nafcillin
Oxacillin
Methicillin
Dicloxacillin
Cloxacillin
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12
Q

what is another name for the Penicillinase Resistant Penicillins

A

Antistaphylococcal PCNs

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13
Q

why were the Penicillinase Resistant Penicillins developed?

A

to overcome the penicillinase enzyme of staphylococcus aureus

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14
Q

what drugs are aminopenicillins

A

ampicillin

amoxicillin

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15
Q

what drugs are carboxypenicillins

A

ticarcillin

carbenicillin

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16
Q

why were the aminopenicllins developed?

A

developed in response to the need for agents with some gram negative activity

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17
Q

why were the carboxypenicillins developed?

A

developed in response to the need for agents with some gram negative activity

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18
Q

what drugs are ureidopenicillins

A

Piperacilin, Azlocillin, Mezlocillin

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19
Q

why were the ureidopenicillins developed?

A

developed in response to the need for agents with some gram negative activity

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20
Q

what drugs are beta lactamase inhibitors

A

sulbactam, clavulanate, tazobactam, avibactam

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21
Q

PCN and Absorption:
Many penicillins are degraded by _______
Lower concentrations are seen with PO PCN – therefore they should only be used when the infection is _________

A

degraded by gastric acid

mild - moderate infections

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22
Q

PCN and Distribution:

True or False: PCNs and beta lactamase inhibitors get into the CSF well very well

A

False!! beta lactamase inhibitors do not

PCNs will get into CSF when doses are high enough!!

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23
Q

PCN and Elimination:

PCNs are usually eliminated by the kidney what PCNs are NOT eliminated by the kidney and how are they eliminated

A

Nafcillin and Oxacillin are eliminated by the LIVER

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24
Q

what PCN preparations have a heavy sodium content

*careful with CHF and Renal Insufficiency patients

A 
sodium PCN G
Nafcillin 
carbencillin
Ticarcillin (most per gram)
Piperacillin
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25
Q

which PCN type should definitely NOT be used for staph infections

A

natural penicillins (so much resistance has been created against them!!)

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26
Q

what PCN types are possibly good for Pseudomonas infections

A

Carboxypenicillins and Ureidopencillins

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27
Q

What are some PCN ADEs?

A

Neurologic
Hematologic
GI
Interstitial Nephritis

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28
Q

What are the Neurologic PCN ADEs?

A

Irritability, jerking, confusion, and SEIZURES

seen a lot when renal insufficiency and high doses

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29
Q

What are the hematologic PCN ADEs?

A

Neutropenia, Thrombocytopenia!!

Hemolysis or anemia

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30
Q

Neutropenia and Thrombocytopenia from PCN usually happens with ______ therapy and is (reversible or irreversible?) with discontinuation

A

happens with prolonged therapy > 2 weeks

is reversible with discontinuation

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31
Q

what is interstitial nephritis

A

immune mediated damage to the renal tubules – seen by an abrupt increase in SCr
and can lead to RENAL FAILURE

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32
Q

Interstitial nephritis seen most commonly with what PCNs?

A

Methicillin (why removed from market)
and
Nafcillin

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33
Q

what drug(s) are monobactams?

A

aztreonam

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34
Q

what drug(s) are 1st gen cephalosporins (that we need to know)

A

Cefazolin

Cephalexin

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35
Q

what drug(s) are 2nd gen cephalosporins (that we need to know)

A

Cefuroxime
Cefoxitin
Cefotetan
Cefprozil

(“Fur” on a “Fox”
and “fot” the “proz”?
IDK?)

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36
Q

what drug(s) are 3rd gen cephalosporins (that we need to know)

A

Ceftriaxone
Ceftazidime
Cefpodoxime

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37
Q

what drug(s) are 4th gen cephalosporins (that we need to know)

A

Cefepime

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38
Q

what drug(s) are the Anti - MRSA cephalosporins (that we need to know)

A

Ceftraroline

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39
Q

what drugs are carbapenems

A

Imipenem, Mereopenem, Ertapenem, Doripenem

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40
Q

what are examples of Cephalosporins with beta lactamase inhibitors

A

Ceftolozane-tazobactam

Ceftazidime-Avibactam

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41
Q

what is an example of carbapenem + a beta lactamase inhibitor

A

meropenem-vaborbactam

imipenem–relebactam

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42
Q

PCN vs Cephalosporins:
which has a 5 membered ring and which one has a 6 membered ring next to the beta lactam ring

and what does that difference cause

A

5 membered: PCN
6 membered: Ceph

the 6 membered ring provides some stability against beta lactamase enzymes

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43
Q

what are cephamyacins

A

a cephalosporin with a methoxy group at position 7 of beta lactam ring AKA the have activity against anaerobes like bacteroides!!! (aka the BDA - below diaphragm aneraobes)

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44
Q

Cephalosporins:
Time dependent or concentration dependent?
Bacteriostatic or Bacteriocidal?

A

time dependent

-cidal!!

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45
Q

1st Gen Cephs:
have the most activity against Gram (positive or negative) aerobes than compared to the other Gram type and when compared to other gens of ceph

A

positive

out of all gens of Cephs – 1st is best for Gram positive aerobes!

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46
Q

As you go from 1st gen to 4th gen Cephs:
they lose _______ activity and gain _____ activity

also you gain ______ stability

A

lost Gram positive; gain Gram negative

gain beta lactamase stability

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47
Q

what gram negative aerobes does 1st gen cephs cover

A

PEK

Proteus, E. Coli, Klebsiella

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48
Q

cephamyacins are a part of what generation of cephalosporins

A

2nd gen

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49
Q

what drugs are cephamyacins

A

cefoxitin
cefotetan
cefmetazole

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50
Q

what gram negative aerobes do 2nd Gen cephs cover

A

HENPEK
Haemophilus, Enterobacter, Neisseria
+
(Proteus, E. Coli, Klebsiella)

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51
Q

Cephamyacins are useful due to their activity against (aerobes or anaerobes)

A

anaerobes!! like Bacteroides

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52
Q

What 2 drugs are the only cephalosporins that have activity against PRSP (penicillin resistant Streptococcus pneumoniae)

A

Ceftriaxone
Cefotaxime
*these are 3rd gen cephs!!

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53
Q

3rd gen Cephalosporins cover what gram negative aerobes?

A 
HENPECKSSS
(Haemophilus, Enterobacter, Neisseria)
\+
(Proteus, E. Coli, Klebsiella)
\+
Citrobacter
\+ 
Serratia, Salmonella, Shigella
and Pseudomonas!!!!!
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54
Q

3rd gen Cephs: good or poor activity against anaerobes

A

poor!!!

2nd gens/cephamyacins are good for anaerobes - but not 3rd gen

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55
Q

what 3rd gen cephs cover Pseudomonas??

A

Ceftazidime

Cefoperazone

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56
Q

the 4th gen ceph (_______)
has similar gram positive coverage as Ceftriaxone (a 3rd gen)
and similar coverage for gram negative aerobes as 3rd generation *most notably this 4th gen drug will cover what 3 bugs?

A

Cefepime;

3 bugs: Pseudomonas!! annnd
beta lactamase producing Enteroabcter and E. Coli

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57
Q

3rd gen or 4th cephs are pretty strong inducers of ESBLs/AmpC?

3rd gen or 4th cephs are weak inducers of ESBLs/AmpC?

A

strong inducers = 3rd gen

weak inducers = 4th gen

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58
Q

Ceftaroline:

it is an Anti _______ Cephalosporin

A

MRSA!

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59
Q

T or F: Ceftaroline will cover Pseudomonas

A

false!!!

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60
Q

The combo cephalosporins and beta lactamase inhibitors spectrum of activity:
Gram + coverage: cover against ______
Gram - coverage: cover against ______

A

+: streptococci

-: similar to Cefepime + some AmpC producing Pseudomonas!!

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61
Q

Overall cephalosporins will not be active against what 3 bugs?

A

MRSA (exept cetaroline)
Enterococcus
Legionella
C.Diff

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62
Q

T or F: None of the cephalosporins reach the CNS

A

false! some do!

3rd and 4th gen parenteral ones do as well as parenteral cefuroxime

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63
Q

what cephalosporings reach the CNS?

A 
Parenteral Cefuroxime (a 2nd gen)
Parenteral 3rd and 4th gen cephs
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64
Q

What cephalosporins do NOT get eliminated by the kidneys

A

Ceftriaxone and Cefoperzone

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65
Q

What cephalosporin does NOT need to be redosed/supplemented post hemodialysis

A

ceftriaxone…

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66
Q

Most cephalosporins have a short half life around 2 hours - which one has a longer half life and how long is the half life

A

Ceftriaxone has a longer 1/2 life - it is around 8 hours and thus can be doses Q12h or Q24h!!!!

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67
Q

what ceph is drug of choice for surgical prophylaxis?

A

Cefazolin

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68
Q

T or F: 1st gen cephalosporins cannot reach CNS/should not be used for mennigitis

A

true

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69
Q

what ceph is used as a single IM dose for uncomplicated gonorrhea

A

ceftriaxone

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70
Q

Hypersensitivity rxns to cephalosporins occur most frequently in pts with PCN allergy — cross reactivity rate is ___ - ___ %

A

5 - 15%

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71
Q

can you give a cephalosporin to someone with a PCN allergy?

A

give with caution if pt has had just rash/pruritis

if anaphylaxis rxn then NOOOO!!

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72
Q

Some cephalosporins have a NMTT side chain that can cause what two ADEs

A 
hypoprothrombinemia (at higher risk for bleeding - bc low vit k production from bacteria in gut)
Disulfiram rxn (alcohol intolerance)
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73
Q

what are some hematologic ADEs of cephalosporins?

how do they happen and how to fix them?

A

Leukopenia, Neutropenia, Thrombocytopenia

occurs mainly in pts getting > 2 weeks of therapy - will be reversed when therapy is discontinued

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74
Q

what are some GI ADEs of cephalosporins?

A

biliary sludging (esp. ceftriaxone therapy)
N/V
transient liver enzyme increase
Pseudomembranous colitis

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75
Q

Can cephalosporins cause seizures?

A

Yepppp

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76
Q

Carbapenems - are they bactericidal or bacteriostatic?

A

bacteriocidal EXCEPT not for enterococcus

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77
Q

T or F: Carbapenems are currently the most broad spectrum abx

A

true

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78
Q

what drug class is drug of choice for ESBL and AmpC producing bacteria

A

carbapenems

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79
Q

which carbapenem does NOT cover pseudomonas

A

ertapenem

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80
Q

T or F: Carbapenem will cover anaerobes

A

true!!! they do super well for anaerobes too

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81
Q

What things to Carbapenems NOT cover

A

MRSA
C.Diff
Atypical Bacteria
Stenotrophomonas maltophilia

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82
Q

which carbapenem gets into CSF best?

A

meropenem

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83
Q

which carbapenem has the longest half life out of the 4 of them?

A

ertapenem (4 hrs)

compared to others of 1 hr 1/2 life)

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84
Q

T or F: only 2 of the 4 carbapenems need renal adjustment when renal dysfunction

A

false! all 4 do…..

they would all be given AFTER hemodialysis because they would be removed

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85
Q

Imipenem gets hydrolyzed by the kidneys by the ______ enzyme and can make it inactive/or maybe nephrotoxic.

A

DHP

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86
Q

Imipenem is given with a DHP inhibitor called __________ to protect against nephrotoxicity by preventing renal metabolism

A

cilastatin

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87
Q

Do carbapenems have cross reactivity to people with PCN allergies?

A

yes (same as cephs: 5 - 15%)

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88
Q

what are some CNS ADEs of carbapenems?

A

insomnia, agitation, confusion, dizziness, hallucinations, and depression
and SEIZURES

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89
Q

Aztreonam is active against which of the following?
Gram + aerobes
Gram - aerobes
Anaerobes

A

ONLY gram - aerobes!!

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90
Q

T or F: Aztreonam covers pseduomonas strains

A

true!! (it is a gram - aerobe!)

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91
Q

Does aztreonam enter the CSF?

A

yes

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92
Q

does aztreonam have the same hypersensitivity risk as cephs and carabapenems if pt has a PCN allergy

A

no!

aztreonam is ok if pt has PCN allergy

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93
Q

Gram Stain Results:
Gram + = _________ color
Gram - = ______ color

A 
\+ = purple
- = red
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94
Q

Gram - or gram + bacteria has a periplasmic space

A

negative

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95
Q

T or F: drugs can penetrate out layers of the cell wall in gram + bacteria effectively

A

true!!

cannot get through gram NEGATIVE (drugs use porins there)

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96
Q

Transpeptidase Reaction for Peptidoglycan making:

The enzyme creates a bridge between ______ and _____; the bridge normally consists of 5 _______ (a type of amino acid)

A

between L-Lys and D-Ala

5 glycine residues

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97
Q

MOA of Beta lactams:
Beta lactams inactivate the enzyme by _______ the transpeptidase ____ residue in the enzyme active site - this forms a stable product = inactivates the enzyme

A

acylating; serine residue

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98
Q

why do bacterial transpeptidases NOT catalyze reactions with host cell proteins?

A

humans do NOT have D-Ala amino acid residues

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99
Q

why are penicillins so reactive?

A

the beta lactam ring is 90 degrees/aka a square and that is not comfortable for the molecule…
the =O part is more like a ketone carbonyl because the Nitrogen next to it that could donate electrons and help is not at a good angle to donate electrons

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100
Q

Beta Lactamases:

How do they modify beta lactams?

A

cut open the ring – the ring canNOT be fixed/put back together

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101
Q

Beta Lactamases:

When they inactivate beta lactams - is the enzyme stuck to drug or does the enzyme get regenerated?

A

it gets regenerated!! via water rxn

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102
Q

How do beta lactams cause allergenicity?

A

the abx act as a HAPTEN;

ACYLATE host cell proteins (this will cause a raise in antibodies)

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103
Q

T or F: you can structurally manipulate beta lactams to get rid of the allerginicity

A

false!!!

the allergenicity comes from the pharmacophore (aka cant change it or da drug wont work)

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104
Q

PCN Degradation:
when in acidic conditions - what are the degradation products
vs
when in basic conditions - what are the degradation products

A

acidic: benzylPENICILLENIC acid, benzylPENILLIC acid, and benzylPENICILLOIC acid
basic: benzylPENICILLOIC acid

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105
Q

T or F: hydrolysis of beta lactams is irreversible

A

true!!!

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106
Q

T or F: hydrolyzed penicillin products have some antibiotic activity

A

false!! no abx activity

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107
Q

What orgo nonsense can help stabilize penicillin from hydrolysis in acidic conditions

A

an ELECTRONEGATIVE substituent on side chain carbonyl will reduce the nucleophilicity of the side chain

108
Q

PCNs that are hydrophillic or lipophillic will have high protein binding
and higher protein binding will cause ______ bioavailability

A

lipophillic;

lower bioavailability

109
Q

PCNs are rapidly excreted by the renal route:

most of the excretion is by glomerular filtration or by tubular secretion

A

tubular secretion is the main mode

110
Q

Tubular Secretion: two mechanisms - one for anions and one for cations: PCNs are anionic or cationic?

A

anionic

111
Q

Since PCNs are anionic — if the drug ______ is given with the PCN it will increase the half life of the drug by anion competition

A

probenecid

112
Q

T or F: PCNs get into the CSF

A

true!

113
Q

what drug(s) are glycopeptides

A

vancoymyocin

114
Q

what drug(s) are streptogramins

A

Synercid (quinupristin-dalfopristin combo)

115
Q

what drug(s) are oxazolidinones

A

Linezolid (Zyvox)

Tedizolid

116
Q

what drug(s) are Lipopeptides

A

Daptomyocin

117
Q

what drug(s) are Lipoglycopeptides

A

Tlavancin
Dalbavancin
Oritavancin

118
Q

MOA of Vancomyocin

A

inhibits synthesis/assembly during second stage of cell wall synthesis by firmly binding to D-Ala-D-Ala aka will prevent cross-linking/elongation of peptidoglycan

119
Q

MOA of Synercid

A

they both bind to the 50S ribosomal subunit to inhibit early and late stages of bacterial protein synthesis

120
Q

MOA of the Oxazolidinones

A

bind to 50S ribosomal subunit byt eh 30S subunit = INHIBITS 70s initiation complex for PROTEIN SYNTHESIS

121
Q

MOA of Daptomyocin

A

inserts its lipophilic tail into the cell wall and makes a transmembrane channel –> leakage of cellular contents and rapid depolarization of the membrane potential leading to inhibition of protein/DNA/RNA synthesis

122
Q

MOA of Lipoglycopeptides

A

act a lot like vanco - they interfere with polymerization/cross linking of peptidoglycan by binding to D-Ala-D-Ala
ALSO oritavancin and telavancin have a lipophillic tail that can puncture a whole in the cell wall just like daptomyocin

123
Q

MOR of vancomyocin

A

modification of the D-Ala-D-Ala vanco binding site of the peptide side chain of peptidoglycan precursors by expression of VanA gene (D-Ala-D-Ala –> D-Ala-D-Lac)

Also VISA happens due to thickening of peptidoglycan layer of the cell wall

124
Q

MOR of Synercid

A

alteration in ribosomal binding site
- encoded by the erm gene

or enzymatic inactivation

125
Q

MOR of vancomyocin: usually encoded by gene ______
vs
MOR of Synercid: usually encoded by gene ______

A

vanc: VanA
Synercid: erm

126
Q

MOR of Oxazolidinones

A

alteration of ribosomal subunit target site (v rare)

127
Q

MOR of Daptomyocin

A

rarely seen but due to altered cell membrane binding through loss of a membrane protein

128
Q

MOR of Lipoglycopeptides

A

alteration in peptidoglycan terminus (especially VanA resistance) (aka D-Ala-D-Ala goes to D-Ala-D-Lac)
*seen with telavancin and dalbavancin (this mode of resistance has not seem to affect oritavancin)

129
Q

PK Notes about Vancomyocin:
Bioavailabiity: Goor or Poor?
1/2 Life: short or long?
CSF Penetration?

A 
awful bioavailability (like nothing absorbed systemically)
1/2 life ~ 6 - 8 hours but can be prolonged to 7 - 14 days in ESRD!!!
CSF: "variable penetration" - so no??
130
Q

PK Notes about Vancomyocin:
Route of Elimination?
Renal adjustment?
Removed during hemodialysis?

A

Route: kidneys via glomerular filtration
Renal adjustment for sure
Vanc is somewhat removed by HD (such a big molecule but some is removed)

131
Q

T or F: Vancomyocin is widely distributed into body tissues

A

true!! goes into adipose tissues a lot

132
Q

when is it best to take a peak concentration of vanc and why?

A

ONE HOUR after end of infusion — want to make sure the drug has had enough time to distribute

133
Q

what weight should be used for dosing vanc and why/

A

use TBW (total body weight) because since drug goes into adipose tissue (need to account for the adipose tissue that may be present)

*exception if > 120 kg then may overdose them with vanc

134
Q

PK Notes about Streptogramins:
Bioavailabiity: Goor or Poor?
1/2 Life: short or long?
CSF Penetration?

A

poor - only available parenteral
short 1/2 life (~ 1 hr..)
minimal penetration into CSF

135
Q

PK Notes about Streptogramins:
Route of Elimination?
Renal adjustment?
Removed during hemodialysis?

A

hepatic clearance/CYP enzymes
no renal adjustment; need to liver adjustments tho
probs not removed with HD? (not sure)

136
Q

PK Notes about Oxazolidinones:
Route of Elimination?
Renal adjustment?
Removed during hemodialysis?

A

elim: renal and non renal ways…
NO renal adjustment needed
Linezolid IS removed by HD; Tedizolid is NOT removed by HD

137
Q

PK Notes about Oxazolidinones:
Bioavailabiity: Goor or Poor?
1/2 Life: short or long?
CSF Penetration?

A

amazing bioavailbility!! 100% for linezolid; 91% for tidezolid
t1/2 life: ~ 5 for linezolid; ~ 12 for tedizolid
CSF: ~30% get to brain…. :( ?

138
Q

PK Notes about Daptomyocin:
Bioavailabiity: Goor or Poor?
1/2 Life: short or long?
CSF Penetration?

A

bioavail: ONLY IV
1/2 life ~ 8 hrs… IS PROLONGED IN RENAL DYSFUNCTION
CSF - not sure….

139
Q

PK Notes about Daptomyocin:
Route of Elimination?
Renal adjustment?
Removed during hemodialysis?

A

eliminated by KIDNEYS
yes! renal adjust
not sure about HD

140
Q

PK Notes about Lipoglycopeptides:
Route of Elimination?
Renal adjustment?
Removed during hemodialysis?

A

Elim: Kidneys for telvancin – not super sure on others??
Adjustment for Telvancin and Dalbavancin
None removed by HD

141
Q

PK Notes about Lipoglycopeptides:
Bioavailabiity: Goor or Poor?
1/2 Life: short or long?
CSF Penetration?

A

only given IV so probably poor
t1/2:Telvancin: ~ 8 hours; the other 2 are like over 200 hours…..
poor, poor CSF penetration`

142
Q

Major ADEs of Vancomyocin?

A 
Red Man Syndrome (infusion reaction)
Nephrotoxicity and Otoxicity
Dermatologic rxns
Hematologic 
Thrombophlebitis
143
Q

for Vancomyocin: what is the preferred route of administration for systemic infections

A

infusion/IV

NOT IM and NOT Oral

144
Q

what is the DOC for C.diff colitis

A

ORAL vanc

NOT IV!

145
Q

what is red man syndrome

A

a side effect seen with Vanc and Lipoglycopeptides; it is flushing.pruritis, and rash on face/neck/upper extremities; vasodilation/hypotension occurs

146
Q

how to manage/treat red man syndrome

A

SLOW DOWN THE INFUSION! *For Vanc: MAX 15 mg per minute!

may give antihistamines/corticosteroids prior to infusion

147
Q

Vanc Nephrotoxicty/Ototoxicty: seen mostly as (monotherapy or polytherapy?)

A

polytherapy!

esp. when a contaminant nephrotoxin or ototoxin

148
Q

Vanc Nephrotoxicty/Ototoxicty:

Which one is reversible upon discontinuation and which one is irreversible

A

Nephro: reversible
Ototox: irreversible

149
Q

what things can indicated nephrotoxicity from Vanc

A

transient elevated in BUN or SCr; sometimes granualr casts in the urine

150
Q

what things can indicated ototoxicity from Vanc

A

tinnitus and high frequency hearing loss may precede onset of deafness

151
Q

Vanc:
Time or Concentration Dependent?
Bactericidal or Bacteriostatic?
Fast or slow killer?

A

TIME
-Cidal
so damn SLOW

152
Q

Synercid:
Time or Concentration Dependent?
Bactericidal or Bacteriostatic?

A

Time dependent

-static (can be cidal if right conditions…)

153
Q

which gram positive abx is a CYP3A4 inhibitor

A

Synercid

154
Q

what drug-drug interactions of concern with Synercid

A

Synercid = CYP3A4 inhibitor

Concerned about Statins, Cyclosporine, Tacrolimus, and Carbamazepine

155
Q

Vanc or Synercid has a significant PAE

A

Synercid

156
Q

ADEs of Synercid

A

Venous irritation/phelbitis
Myalgias/Arthralgias
GI (N/V/D)

157
Q

Oxazolidinones:

Bacteriostatic or Bacteriocidal?

A

-static

158
Q

Oxazolidinones or Daptomyocin has a PAE?

A

Oxazolidinones

159
Q

Oxazolidinones:

which one is pulled of by Hemodialysis?

A

linezolid

160
Q

Drug interactions with Oxazolidinones?

and why?

A

SSRIs!!

Oxazolidinones are weak inhibitors of monoamine oxidase – can lead to increase risk of serotonin syndrome

161
Q

ADEs of Oxazolidinones:

A

GI
CNS
THROMBOCYTOPENIA/ Anemia

162
Q

ADEs of Daptomyocin

A 
Myopathy/CPK elevation
Acute Eosinophilic Pneumonia***
GI/Headache
Injection site rxns
Rash
163
Q

Drug interactions with Daptomyocin?

A

statins!! bc increased risk of myopathy

164
Q 
Lipoglycopeptides:
Which one(s) need renal adjustment?
A

Telavancin
Dalbavancin

(NOT oritavancin)

165
Q 
Lipoglycopeptides:
which one(s) have a super long 1/2 life
A

dalbavancin

oritavancin

166
Q

ADEs of lipoglycopeptides

A

Red man Syndrome
Nephrtoxic
QTc Prolongation
Taste Disturbances

167
Q

Pregnancy Category for Lipoglycopeptides

A

Telavancin

168
Q

MOA of aminoglycosides:

A

inhibit protein biosynthesis - by binding to 30S ribosomal subunit
will impair proofread function –> nonsense proteins –> messes with cell wall function –> leakage

169
Q

How are aminoglycosides taken up cellulary?

A

through cytoplasmic membrane active transport process

done by displacement of Mg2+/Ca2+ ions

170
Q

3 Resistance Mechanisms of for aminoglycosides

A
  • BACTERIA will inactivate aminoglycosides (via acetylation, adenylation, phosphorylation)
  • Altered ribosomes
  • Altered aminoglycoside uptake
171
Q

Toxicities of aminoglycosides?

A

Ototoxicity and Nephrotoxicity

Curare-Like effects: Respiratory paralysis

172
Q

Likelihood of aminoglycoside toxicity is increased when what?

A

if therapy > 5 days; if elderly, if renal function is impaired, and higher doses

173
Q

T or F: Aminoglycosides and beta lactams should be administered in the same arm to increase synergistic effects

A

FALSE! do not put in same arm!! (they could mix and have a chemical rxn) also do not mix together in same solution!!

174
Q

Aminoglycosides: typically used for Gram + or Gram - bacteria?

A

Gram -

175
Q

what drugs are aminoglycosides

A 
Amikacin
Tobramycin
Gentamicin
Neomycin
Paromomycin
Streptomyocin
Plaxomicin
176
Q

What drugs are macrolides

A

Erythromycin
Clarithromycin
Azithromycin

177
Q

what was the 1st drug that could be used to treat tuberculosis

A

Streptomycin

178
Q

what aminoglycosides are orally used

A

Neomycin B

Paromomycin

179
Q

why would oral aminoglycosides be used

A

suppress gut flora for travelers diarrhea and for GI surgery prophylaxis

180
Q

Macrolide abx are known as macrocyclic ______

A

lactones

181
Q

What is the sugar called that is important for activity for macrolides

A

desosamine sugar

182
Q

what antibiotic is known as a polyketide?

A

macrolides

183
Q

what is a polyketide?

A

alternating methyl groups!

due to sequential addition of propionate groups to a growing chain

184
Q

MOA of Macrolides

A

inhibit bacterial protein synthesis: bind to the P site of the ribosome/inhibits translocation of peptidyl tRNA from “A” to “P” site

185
Q

what are the 4 resistance mechanisms against Macrolides

A
  • Lactone Ester hydrolase
  • RNA methylase drug induced production (the A2058 adenine base gets methylated)
  • A2058 site: the adenine gets mutated to a guanine (decreases binding by the abx insanely well)
  • efflux pump
186
Q

what drug class gets inactivated by acidic conditions and turns into a ketal formation

A

Macrolides

187
Q

Why is oral erythromycin put in an enteric coated tablet?

A

to prevent it from getting degraded by acidic conditions

188
Q

The ketal reaction product form erythromycin in an acid environment is inactive and causes what side effect

A

GI cramping

189
Q

which macrolide is not possibly able to be made into the inactive ketal shape and why

A

azithromycin because the O= is actually a N=CH3 (aka not possible… bc orgo science)

190
Q

main route of erythromycin elimination

A

demethylation by the liver

191
Q

drug interactions for macrolides

A

they inhibit CYP3A…

thus Drug interactions with CBZ, cyclosporine, disopyramide, quinidine, theophylline, digoxin

192
Q

Odd side effects of Macrolides

A

Stevens Johnson Syndrome
Reversible cholestatic hepatitis –> jaundice
Pyloric Stenosis in kids that mothers used it while pregnant

193
Q

Aminoglycosides (AGs):

T or F: need to individually dose for every patient

A

true (bc narrow therapeutic index)

194
Q

AGs:

(polar or non polar) compounds and thus are (soluble or non soluble) in water

A

polar;

soluble

195
Q

AGs:
good or poor oral aborption?
good or poor CNS penetration?
good or poor lung penetration?

A

poor and poor and poor (because they are so polar!!)

196
Q

what drugs are aminoglycosides?

A

Gentamicin
tobramycin
Amikacin
Streptomycin

197
Q

MOA of AGs?

A

irreversibly bind to 30s ribosomal subunit = stop protein synthesis

198
Q

AGs:
Slow or fast killers?
Bacteriocidal or Bacteriostatic?
Time or Concentration dependent killer

A

so fast!!
-cidal!
concentration

199
Q

AGs:
Get through outer membrane of Gram negative cells via porins, once in the periplasmic space - how do they get across the inner membrane?

A

get through via MEMBRANE potential/ energy dependent

200
Q

AGs:
getting through the inner membrane in gram negative cells require ________ and ______ (thus they are not helpful for ________ bugs)

A

require: energy and OXYGEN

since needs Oxygen - not good for ANAEROBES

201
Q

AGs:
inner membrane transport requires energy and thus is the rate limiting step:
what things can IMPAIR transfer across the membrane

A

hyperosmolarity, divalent CATIONS, low pH (more H+), or anaerobiasis
anything that makes the inside of the cell more positive will hinder transport..

202
Q

MOR for AGs?

A

Synthesis of AG modifying enzymes (plasma mediated)

Alteration in ribosomal binding sites (rare)

203
Q

Which aminoglycoside is “usually” not affected by AG modiyfing enzymes

A

amikacin

204
Q

why is the MOR of alteration in ribosimal binding sites rare

A

because the AGs bind to multiple sites

205
Q

Pk/PD parameter for AGs?

and the goal value?

A

PEAK: MIC;
10:1 is optimal

206
Q

AGs can NEVER be used alone for what infections?

A

when Gram + aerobes - NEVER US ALONE - dose with cell active agents

207
Q

AGs should use higher doses for what kinds of infections?

A

for Gram - aerobes

208
Q

AGs do not cover what types of bugs at all?

A

anaerobes

209
Q

Streptomyocin will cover what type of bacteria?

A

Mycobacteria - TUBERCULOSIS

210
Q

AGs have synergy with what agents?

A

cell wall active agents: beta lactams and vanco

211
Q

T or F:

AGs have PAE

A

truee

212
Q

what two patient variables are important for AG dosing

A

Volume of distribution
&
Clearance

213
Q

why should IM injections of AGs NOT be used in critically ill pts

A

critically ill pts = hypotensive = no good perfusion the muscle to disperse the drug

214
Q

T or F:

AGs distributes heavily to the adipose tissue

A

false!!!

goes to extracellular fluid more NOT adipose tissue (or CSF or sputum)

215
Q

For AGs: TBW or IBW/LBW should be used

A

IBW! (use AdjBW if > 130% if IBW)

TBW is for Vanc

216
Q

for AGs: use a higher of lower Vd when patient has edema (HF, CKD, hepatic ascites patients)

A

higher Vd: more fluid = higher Vd!

217
Q

T or F:

AGs do not renal adjustment

A

false!! they do

218
Q

T or F:

Give supplemental AG doses post Hemodialysis

A

trueee

219
Q

what AGs are good for Gram negative aerobic bacteria
vs
what AGs + are good for enterococci, viridans streptococci, staphylcocci (aka Gram +)

A

Negative: Amikacin, Gentamicin, Tobramycin

Positive: use Gentamicin or Streptomycin WITH a cell wall active agent!!

220
Q

ADEs with AGs?

A

nephrotoxicty and ototoxicity!!!

221
Q

what are the risk factors of getting nephrotoxicity or ototoxicity with AGs

A 
PROLONGED TROUGH CONCENTRATIONS
prolonged therapy (> 2 weeks)
underlying renal insufficiency
advanced age
hypovolemia
use of contaminant nephrotoxins or ototoxins
222
Q

what drugs contaminant drugs could cause ototoxicty with AGs

A

Loop diuretics - furosemide

Vancomyocin

223
Q

what drugs contaminant drugs could cause nephrtoxicty with AGs

A

vancomyocin
amphoterocin B
cisplatin
CT contrast

224
Q

what drugs are macrolides

A

erythromycin
azithromycin
clarithromycin

225
Q

the chemical modifications for clarithromycin and azithromycin have led to what improvements when compared to erythromycin

A
  • better tolerated by patients
  • enhance spectrum of activity
  • improve tissue penetration
  • longer elimination 1/2 lives
226
Q

MOA of Macrolides?

A

reversibly bind to 50S ribosomal subunit: will inhibit protein synthesis

227
Q

Macrolides:
time or concentration dependent?
bacteriocidal ot bacteriostatic?

A

time

-static!

228
Q

MOR of Macrolides?

A

active efflux by “mef” gene

alteration in binding site by “erm” gene

229
Q

the erm gene causes resistance via what mechanism

A

methylation to 50s binding site/altered ribosomal binding site

230
Q

when the erm gene is active - what drugs are affected by resistance

A

macrolides
clindamycin
synercid
(bc all bind to 50S binding site)

231
Q

Macrolides:

what notable organisms do they NOT cover

A

NOT PRSP, MRSA< or Enterobacteriaceae

232
Q

what 3 drug classes DO cover atypical bacteria

A

Fluroquinolones
macrolides
tetracyclines

233
Q

T or F:

Macrolides cover anaerobes

A

true!

“above the diaphragm”

234
Q

which macrolide(s) have lower bioavailability when food is present

which macrolide(s) bioavailability is not affected if food is present

A

lower bioavail: erythromycin

not affected: clarithromycin, azithromycin

235
Q

Macrolides:
Get into CSF well?
Get into tissues well?
Get into serum/systemic system well?

A

CSF: NO
Tissues: YES
Serum: NO –> NOT GOOD FOR BACTEREMIA

236
Q 
Macrolides:
which macrolide(s): needs renal adjustment when CrCl < 30 mL/min
A

renal: clarithromycin

237
Q 
Macrolides:
which macrolide(s): are CYP450 inhibitors
A

erythromycin

clarithromycin

238
Q 
Macrolides:
which macrolide(s): is NOT known to be associated with CYP450 drug-drug interactions
A

azithromycin

239
Q

ADEs of Macrolides:

A 
GI: epigastric distress (like acid burn)
Cholestatic hepatitis 
Thrombophlebitis/infusion site irritaiton
Allergic Rxns
Ototoxicity
QT prolongation
240
Q

Macrolides:

which macrolide causes the worse epigastric pain

A

erythromycin

241
Q

what drugs will have the serum levels increase if taken at the same time as erythromycin or clarithromycin

A 
Theophylline
Carbamazepine
Valproate
Cyclosporine
Digoxin
Phenytoin
Warfarin

*if see these drugs – ok to use AZITHROMYCIN THO

242
Q

T or F:

macrolides cover atypical bugs

A

true!!

243
Q

what drugs are Fluroquinolones (FQs)

A

Ciprofloxacin
Levofloxacin
Moxifloxacin
Delafloxacin

244
Q

Original prototype of the FQs

A

nalidixic acid

245
Q

MOA of FQs

A

binding/inhibiting bacterial topoisomerases II and IV

topo II = gyrase

246
Q

FQs:
Gram negative bacteria inhibited by primary target of ________
vs
Gram positive bacteria inhibited by primary target of ________

A

negative: gryase/topo II
positive: topo IV

247
Q

MOR of FQs:

A

alteration in binding sites
active efflux
alteration in cell wall permeability
cross resistance is seen with FQs

248
Q 
FQs:
which FQ(s) are older?
which FQ(s) are newer/"respiratory"
A

older: ciprofloxacin
newer/respiratory: levofloxacin; moxifloxacin,

also Delafloxacin is new and exists

249
Q

Ciprofloxacin:

better for gram positive or negative aerobes

A

gram NEGATIVE

250
Q 
FQs:
which FQs(s) cover MRSA
A

ONLY delafloxacin

251
Q 
FQs:
which FQ(s) cover PRSP
A

ALL

except CIPRO!!!

252
Q 
FQs:
which FQ(s) cover Pseudomonas aeruginosa
A

Cipro, Dela, and Levo

253
Q

which FQ does NOT cover pseudomonas

A

moxifloxacin or gemifloxacin

254
Q

T or F:

FQs have little affect on atypical bacteria

A

FALSE!

they are super good for atypical;

255
Q

FQ(s):
slow or rapid killing?
time or concentration dependent?
PAE - yes or no?

A

RAPID!!
Concentration
yes, PAE

256
Q

FQ(s):

poor or good bioavailability

A

good

257
Q

FQ(s):

do they get into the CSF?

A

yes — when meninges are inflamed

258
Q

T or F:

FQs are not good for UTIs

A

FALSE! they are great for them

EXCEPT moxi and gemi do not get into the urine enough

259
Q

FQ(s):

Renal adjustment - yes or no?

A

yes

*cipro and dela have both renal and hepatic elimination

260
Q

FQ(s):

Removed by HD- yes or no?

A

NOOOO

261
Q

ADEs of FQs

A

GI - CDF
Neurologic: Seizures AND PERIPHERAL NEUROPATHY
QT prolongation
Articular damage – avoid in KIDS and pregnant/breastfeeding pts
Tendonitis/Tendon Rupture
(Phototoxicity — for weird FQs tho)

262
Q

what cardiac related reasons should FQs be used with caution

A

hypokalemia
concomitant use of amiodarone/sotalol (antiarrhythmics)
preexsiting QT prolongation

263
Q

Drug interactions for FQs?

A

divalent/trivalent cations (“ZICAM” - zinc, iron, Ca2+, Al, Mg2+, antacids, sucralfate (has Aluminum), enteral feeds
warfarin

Theophylline and cyclosporine – only with CIPRO

264
Q

what is the issues with warfarin and FQs

A

increasing bleeding risk/longer prothrombin time

265
Q

what are the two drug interactions for FQs that is really only with cipro

A

theophylline

cyclosporine

266
Q

why are divalent/trivalent cations a problem for FQs

A

they chelate to the drug and prevent them from working

267
Q

how to get around the divalent/trivalent cation drug interaction

A

take FQ 2 hours before other drugs
(best to take FQ first – because abx are best)
or take FQ 2 - 6 hours after these agents

PHRM 865 (59 decks)

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