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Clinical Pharmacology I > Bugs & Drugs > Flashcards

Bugs & Drugs Flashcards

1
Q 
Staphylococcus epidermidis
Staphylococcus aureus
Streptococcus A, B, C, G
Streptococcus pneumoniae
Enterococcus faecalis
Enterococcus faceium

What are they?

A

Gram Positive Aerobes

Staph/strep live on the skin.
Enterococcus live in the gut.

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2
Q

Peptostreptococcus sp.
Peptococcus sp.
Clostridium difficile
Clostridium perfringens

What are they?

A

Gram positive Anaerobes

Cocci live in the mouth. When treating animal bites, this bacteria should be covered.
C. diff is a common ADR to Abx. Abx kill off gut flora so C. diff. colonizes (causes cholitis).

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3
Q

Haemophilus influenzae
Moraxella catarrhalis
Salmonella
Shigella

What are they?

A

Wimpy Gram Negatives; very susceptible to antibiotics.

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4
Q

Eschericha coli
Klebsiella pneumoniae
Proteus marabalis
Proteus vulgaris

What are they?

A

Medium Gram Negatives

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5
Q

What are the SPACE bugs?

A 
Serratia marcescens
Pseudomonas aeruginosa
Acinetobacter baumanii
Citrobacter freundi
Enterobacter

Gram negative group that is likely to develop resisitance to drugs.

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6
Q

How do you treat MDR pathogen?

A

Use one toxic drug to treat them. Broad spectrum drugs have selective pressure and can create resistant bugs.

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7
Q

Where are anaerobes found?

A

Survive without oxygen; found on normal flora of skin and mucous membranes.

Places of infection: GI, deep puncture wounds, URTI, dental, female genital area, bone.

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8
Q

Where does peptostreptococcus live?

A

Mouth

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9
Q

Where does backteroides and clostridium live?

A

the gut

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10
Q

What are three examples of Atypicals?

A

Chlamydia, Mycoplasma (lack cell wall), Legionella

Do not absorb color with gram stains.
Zoonotic - can be spread by animals.
Most Abx have poor coverage for ATYPICALS.

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11
Q

What is the heteropolymeric component of a cell wall that provides rigid mechanical stability and has cross-linked latticework structures and peptides?

A

Peptidoglycan

Gram NEG have LESS peptidoglycan than GRAM POS.

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12
Q

What is LPS?

A

A rich outer coating in gram negative bacteria; makes it more difficult to treat.

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13
Q 
Bacteria by Site of Infection:
Staphylococcus aureus
Staphylococcus epidermidis
Streptococcus pyogenes
Pasteurella spp.
A

Skin/soft tissue

Lots of Gram POS and some anaerobes.

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14
Q 
Bacteria by Site of Infection:
Staphylococcus aureus
Staphylococcus epidermidis
Streptococcus spp.
Neiserria gonorrheae
Gram negative rods
A

Bone and Joint
Mostly gram positive.
Infection is bad when there’s gram negative rods appearing. I/C pt can have atypicals (Neisseria).

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15
Q 
Bacteria by Site of Infection:
Streptococcus pneumoniae
Neisseria meningitidis
Haemophilus influenzae
Group B streptococcus
Listeria spp.
E. Coli
A

Meningitis

Gram POS and NEG

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16
Q 
Bacteria by Site of Infection:
E. Coli
Proteus spp
Klebsiella spp.
Enterococcus spp. 
Bacteroides spp.
A

Abdomen

Mostly anaerobes

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17
Q 
Bacteria by Site of Infection:
E. coli
Proteus spp.
Klebsiella spp.
Enterococcus spp. 
Staphylococcus saprophyticus
A

Urinary Tract = need gram neg coverage.

Catheters have increased risk of infection, so Gram POS may appear.

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18
Q

Bacteria by Site of Infection:
Peptococcus spp.
Peptostreptococcus spp.
Actinomyces spp.

A

Mouth

Land of anaerobes

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19
Q 
Bacteria by Site of Infection:
S. pneumoniae
H. influenzae
Moraxella catarrhalis
Streptococcus pyogenes
A

Upper Respiratory Tract - gram positives and negatives

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20
Q 
Bacteria by Site of Infection:
S. pneumoniae
H. influenzae
K. pneumoniae
Legionella
Mycoplasma pneumoniae
Chlamydia pneumoniae
A

Lower Resp. Tract (Community acquired)

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21
Q 
Bacteria by Site of Infection:
MRSA
Pseudomonas aeruginosa
Enterobacter spp.
K. pneumoniae
Serratia spp.
A

Lower Resp. Tract (NOSOCOMIAL)

SPACE BUGS

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22
Q

PK

A

What the body does to the drug!

ADME

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23
Q

PD

A

What the drug does to the body!

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24
Q

What is absorption?

A

How drug enters the blood, which is affected by acid and food. Ex: high fat diet = less absorption.

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25
Q

What is distribution?

A

How drug travels in the bloodstream, which is affected by protein binding. Used to pinpoint med to the site of infection.

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26
Q

What is metabolism?

A

How the body chemically changes the drug to prepare for excretion, which is often affected by other drugs.

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27
Q

What is excretion?

A

How the body gets the drug out; usually stool or urine and is affected by other drugs.

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28
Q

Bioavailability

A

How much of a drug is absorbed.

IV push = 100%.

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29
Q

First pass effect?

A

Can be metabolized by liver before getting into the bloodstream.

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30
Q

The ____ the distribution, the more it’ll be in the tissues.

A

Higher; good for skin infections.

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31
Q

The _____ the distribution, the more drug will be in central circulation.

A

Lower; good for blood infections

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32
Q

What is primary hepatic metabolism?

A

CYP450

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33
Q

What is the most common hepatic metabolism?

A

CYP3A4 - metabolizes HALF of all drugs.

Phase 1 - makes drug polar for excretion to the kidneys or to go to Phase 2 metabolism.
Phase 2 - add onto molecule to make it more polar (i.e. sulfination).

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34
Q

What’s MIC?

A

Minimum concentration of drug needed to visibly reduce the growth of bacteria.

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35
Q

Bactericidal

A

Eradicates infection without host defense mechanisms; KILLS BACTERIA. Good for I/C.

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36
Q

Bacteriostatic

A

Inhibits growth, requires host defense to eradicate infection. DOESNT KILL.

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37
Q

Therapeutic Index

A

Range between toxicity and effective dose. Need to be above the MIC, but not near the lethal dose if there’s a small therapeutic index.

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38
Q

Classes of bactericidal antibiotics?

SIX CLASSES

A

Disrupts bacterial function so much that cell death will occur.

CSNs, Aminoglycosides, PCNs, Vancomycin, Fluroquinolones, Metronidazole

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39
Q

Classes of bacteriostatic antibiotics?

FIVE CLASSES

A

Inhibits a vital pathway used in the growth of bacteria, but doesn’t directly cause death.

Erythromycin, Tetracyclines, Sulfonamides, Trimethoprim, Clindamycin

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40
Q

Synergy

A

Combined activity is greater than either component alone.

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41
Q

Peak

A

Maximum concentration achieved

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42
Q

Trough

A

Minimum concentration achieved; usually lowest and what is hit until administration of next dose.

When QD, it can drop to zero.

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43
Q

AUC

A

Area under curve = Total drug exposure; important for a concentration vs. time dependent killer.

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44
Q

CDK

A

antimicrobial activity directly impacted by how high Cmax is above the MIC. Higher the peak, the better it works.

Even when below MIC, bacteria will not grow for a period of time (Post Abx Effect).

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45
Q

When is a loading dose used?

A

For concentration dependent killers; loading dose is used to get to a steady state quicker.

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46
Q

TDK

A

antimicrobial activity directly related to the time spent above the MIC.
Ex: PCN half life is short – need to be given several times per day.

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47
Q

Risk with TDK?

A

Without continuous infusion, there’s vacillation.

Risk: fall below MIC if you ever miss a dose.

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48
Q

Delay before microorganisms recover and reenter a log-growth period.

Affected by?

A

Post Abx Effect

Affected by size of innoculum, type of growth medium, and bacterial growth phase.

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49
Q

Empiric Therapy

A

Prescribing without knowing causative agent; BSA used.

Cultures come back - switch to a focused antibiotic.

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50
Q

How do you choose a drug?

A
  1. Spectrum of activity - consider the causative organism in location.
  2. PK - Consider patients ADME function.
  3. PD - bacteriostatic or bactericidal? Check immune function.
  4. Toxicity - consider all risks (GI, skin, hematologic, CNS, hepatic, RENAL).
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51
Q

Why are tetracyclines bad for kids?

A

They stain teeth; can’t give to anyone under 8yo.

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52
Q

Why is Chloramphenicol bad for kids?

A

Gray baby syndrome; can’t metabolize it themselves because of their immature hepatic enzymes.

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53
Q

When is combination therapy used?

A

Life-threatening infections; causative agent unknown. Early therapy improves outcomes.

Polymicrobial infections.
Enhance antimicrobial activity.
Treatment of resistant strains.

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54
Q

What is synergistic in pseudomonas aeruginosa infections?

A

Penicillins-Aminoglycosides

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55
Q

Do you take cultures before or after starting antibiotics?

A

Cultures BEFORE - Do not want abx to affect culture results (organism could have died off).

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56
Q

How do we know if abx is effective against bacterium?

A

Greater the zone of inhibition, the more effective at killing.

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57
Q

Resistant bugs

A

GPOS - MRSA, VRE, VRSA
GNEG - ESBL & KPCs

Extended sp. beta lactamase (Kill antibiotics).
Kelebsiella producing carbamases

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58
Q

What practices cause resistance?

A

Indiscriminate abx use
Prolonged hospital stay
Greater than 7 days on mechanical ventilation
Prophylaxis use and BSA.

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59
Q

What is a mechanism of resistance in GNEG bacteria?

A

Plasmid exchange allows bacteria to communicated and share resistance.
Ex: changing PBP so PCN can’t bind. Also can make pumps to clear medicine out of cell.

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60
Q

MOA: Penicillin

A

D-alnine is important for cross linking in the cell wall. B-lactam ring micmics D-alanine and this bond prevents propagation of cell wall.

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61
Q

Allergies to PCN occur where?

A

R-side chain

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62
Q

Beta lactams - Bacteriostatic or Bactericidal?

A

Bactericidal

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63
Q

What do natural PCNs cover?

A

G+, no staph

Anaerobes, no bacteroides

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64
Q

What are PCN’s drug of choice for?

A

Meningococcus, gas gangrene, syphillis

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65
Q

PCNs - TDK or CDK?

A

TDK

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66
Q

Name the natural penicillins and route of administration?

A

PCN G - Given IV.
PCN V Potassium - Oral version, stable in stomach acid because of potassium.
PCN G Benzathine - Given IM; one time dose.

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67
Q

Why do you never push a suspension through an IV line?

A

Risk of emboli.

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68
Q

What do aminoPCNs cover?

A

Ampicillin
Amoxicillin

Cover G+, no staph, AN, no bacteroides

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69
Q

What are aminoPCNs used for?

A

Enterococcus, Listeria, Endocarditis prophylaxis, URI.

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70
Q

Why don’t you give aminoPCN to someone on anticoagulants?

A

Causes abnormal prolongation of PT.

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71
Q

What must you tell a female patient when prescribing aminoPCNs?

A

Decreases effectiveness of birth control, due to loss of enterohepatic recycling of estrogen in the gut.

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72
Q

Side effects of AminoPCNs?

A

Hepatic dysfunction, hepatitis, jaundice, increase in serum AST, ALT, bilirubin, ALP., C.diff possible, SJS and TEN, interstitial nepritis, hematuria, crystalluria, Anemia, thrombocytopenia.

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73
Q

CI of aminoPCN?

A

PMHx of cholestatic jaundice, hepatic dysfunction, allergy

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74
Q

PCN dosing consideration

A

Renal

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75
Q

What labs do you monitor for patients on PCN?

A

Renal, Hepatic, PLT

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76
Q

How do microbes have resistance to PCN?

A

Beta lactamase enzyme cleaves the ring in the antibiotic inactivating it.

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77
Q

What are beta lactamase inhibitors?

A

Chemicals wit no antibacterial activity that inactivate beta lactamase resistant enzyme.

Sublactam and Ampicillin
Tazobactam and Pipericillin
Clauvanate with Amoxicillin

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78
Q

What do AminoPCNs with Beta Lactamase inhibitors cover?

A

GPOS, now with MSSA

Anaerobes PLUS Bacteroides,

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79
Q

AminoPCNs with Beta Lactamase inhibitors are drug of choice for?

A

BITES, skin and soft tissue, diabetic foot, and intra-abdominal infections.

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80
Q

What is another name for PCN-ase Resistant PCNs?

A

Antistaphylococcal PCNs

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81
Q

Name 3 Antistaphylococcal PCNs

A

Nafcillin, Oxacillin, Dicloxacillin

82
Q

Antistaphylococcal PCNs - designed to cover?

A

Cover MSSA and gram positives only.

83
Q

Dosing considerations for Antistaphylococcal PCNs?

What do you monitor?

A

Hepatic FXC

Montor Hepatic, CBC, anaphylaxis.

84
Q

What bug is resistant to Antistaphylococcal PCNs?

A

MRSA

85
Q

What is an Antipseudomonal PCN?

A

Piperacillin/Tazobactam

86
Q

What is piperacillin and tazobactam used for?

A

Pseudomonas treatment! And MSSA.

Covers GPos, An, and GNeg.

87
Q

Piperacillin/Tazobactam is DOC for what?

A

Polymicrobial infections, nosocomial infections, intra-abdominal infections, and pseudomonal infections.

88
Q

Dosing consideration for Antipseud PCNs?

What do you monitor?

A

RENAL

Anaphylaxis, Renal FXC, CBC

89
Q

What type of PCN is effective against MRSA?

A

NONE

90
Q

What type of pt’s would pipericillin and tazobactam be good for? Who would it be a poor choice for?

A

Good for geriatrics from nursing homes who need empiric coverage.
Poor choice for children.

91
Q

MOA: Cephalosporins

A

Act on PBP and cell wall.

92
Q

Cephalosporins have good penetration of what?

A

CSF

93
Q

Why can patients who are sensitive to PCN, be able to take Cephalosporins?

A

PCN cross sensitivity is less than one percent.

94
Q

What cephalosporins have anti-pseudomonal activity?

A

Ceftazadime (FORTAZ) and Cefepime.

95
Q

How are cephalosporins metabolized?

A

Renally

96
Q

What are the 1st generation CS? Coverage?

A

Ancef and Keflex

GPos and some GNeg – Proteus, Klebsiella, E.coli

97
Q

What is Ancef used for?

A

Surgical prophylaxis, MSSA, UTI

98
Q

What is Keflex used for?

A

Skin/soft tissue infections, cellulitis, UTIs.

99
Q

What are the second generation CS? Coverage?

A

Metfoxin
Zinacef
Cefzil

Gram positive and gram negative

100
Q

What are ___ used for?
Metfoxin
Zinacef
Cefzil

A

UTI, URI, surgical prophylaxis.

2nd generation is LEAST used clinically.

101
Q

What are third generation CS? Coverage?

A

Rocephin
Fortax
Claforan

Cover GPos and GNeg; extra coverage against Serratia and Moraxella catarrhalis.

102
Q

Why is Rocephin coverage important?

What two times can’t you use it?

A

Good strep coverage.
Can’t use during first 30 days of life.
Don’t mix with calcium.

103
Q

What drug is preferred for neonatal fever and sepsis From 3rd generation of CS?

A

Claforan

104
Q

Why can’t you use Rocephin during first 30 days of life?

A

It will bind to albumin in neonates and cause toxicity.

The free drug kicks off bilirubin to bind to albumin causing jaundice.

105
Q

What is the 4th generation CS? Coverage?

A

Cefepime (MAXIPIME) - GPos, GNeg only.

Has pseudomonal activity. NO MRSA or enterococcus.

106
Q

What patients would you use Cefepime (Maxipime) for?

A

Good for neutropenic patients, fever, AIDS, chemo patients, hospital acquired pneumonias, and ventilator acquired pneumonias

Nosocomial/pseudomonal cases

107
Q

What is the 5th generation CS? What does it cover?

A

Teflaro - Has GPos, GNeg, and MRSA coverage!
Treats MRSA and pseudomonas.
»Skin infection and CAP

Ceftolozane / tazobactam - GNeg, GPos, NO MRSA or enterococcus.

108
Q

What is Ceftolozane / tazobactam?

A

5th generation CS. Covers Gram Neg and Pos, but doesn’t cover MRSA or eneterococcus.

109
Q

What is ceftolozane and tazobactam DOC?

A

Complicated UTI that failed a round of antibiotics or a complicated abdominal infection with METRONIDAZOLE.

110
Q

How do we use Ceftolozane and tazobactam to treat intra-abdominal infection?

A

It doesn’t cover enough anaerobes, so treats well when paired with METRONIDAZOLE.

111
Q

MOA: Monobactams

A

Inhibit cell wall synthesis; bactericidal.

Aztreonam.

112
Q

What is Aztreonam coverage??

A

Gram negative coverage only; includes enterobacter and pseudomonas.

113
Q

What is the dosing consideration for Teflaro?

A

RENAL

114
Q

What microbes does Teflaro cover?

A

GPos, GNeg, Pseudomonas, MRSA

115
Q

What’s a benefit of a monobactam? Why?

A

Can be used on patients with allergies to PCN. NO cross reactivity with beta-lactams.

116
Q

What are the carbapenems? Name them.

A 
Broad spectrum (no MRSA) - used for resistant infections, like meningitis, VAP, etc. 
>>Susceptible to KPC - Klebsiella producing carbamases.

Imipenem, Meropenem, Ertapenem, Doripenem.

117
Q

Carbapenemds DOC for?

A

MDR GNeg infection (pseudomonas), Extended spectrum beta lactamase producing bacteria (ESBL), nosocomial infections, and meningitis.

118
Q

Monobactam - Dosing considerations? Monitoring?

A

Renal

LFT, symptoms anaphylaxis, diarrhea.

119
Q

What don’t carbapenems cover?

A

MRSA

120
Q

What coverage do they provide?

A

GPos, Neg, and Anaerobes

121
Q

What carbapenem doesn’t cover pseudomonas?

A

Ertapenem

122
Q

What labs are monitored in carbapenems?

A

Renal, hepatic, CBC

123
Q

If your patient is on a carbapenem and has a siezure, which medication will you discontinue?

A

Ertapenem

124
Q

MOA: Vancomycin

A

Cell wall synthesis - inhibits by blocking the cross linking mechanisms by binding to D-alanine. More difficult to develop resistance.

125
Q

Vancomycin coverage? DOC?

A

Gram positive ONLY.

DOC for PCN allergy infections, MRSA, C.diff, endocarditis, osteomyelitis, and surgical prophylaxis.

126
Q

Why does vanco treat C. diff?

A

When taken orally, stays in GI tract to kill infection.

127
Q

Why is vanco used as a surgical prophylaxis when a patient has a PCN allergy?

A

It targets gram positives that are on the skin flora, such as staph and strep.

128
Q

When would you draw a trough for vancomycin? Why?

A

Troughs drawn a half hour before the forth dose to give indication of steady state.

Takes 4-5 half lives to reach steady state.

129
Q

Your patient is receiving vanco Q8hrs, but you check labs and his creatinine is elevated. What is your nexxt move?

A

Space out the dose since the renal clearance has decreased; needs more time to metabolize drug.

130
Q

What types of toxicity does vanco cause?

A

Ototoxicity

Nephrotoxicity

131
Q

What are some infusion related reactions with vancomycin?

A

Red man syndrome
Fever and chills
Phlebitis

132
Q

How do you prevent red man syndrome?

A

Caused by infusing vanco too rapidly, slow infusion rate first.

133
Q

What do protein synthesis inhibitors do?

A

They target the bacterial ribosome to prevent it from making proteins.

134
Q

T/F: All protein synthesis inhibitors are bacteriostatic, except for aminogycosides.

A

True

135
Q

MOA: Macrolides

A

Inhibit protein synthesis by blocking transpeptidation.

136
Q

What are the macrolides?

A

Erythromycin, Clarithromycin, Azithromycin

137
Q

What is the coverage of macrolides?

Why is this significant??

A

GPos aerobles, like S. pneumoniae, MSSA, S. pyogenes, L. monocytogenes.

GNeg aerobes - H influenzae, Mcatarrhalis, N meningitides, N. gonorrhea.

Atypicals - Legionella, Mycoplasma pneumoniae, chlamydophilia pneumoniae, chlamydia trachomatis.

138
Q

Macrolides DOC for?

A

RTI, CAP, AOM, pharyngitis, tonsillitis, bronchitis.

Mycobacterium avium complex for prophylaxis and treatment.

Chlamydia = azi and ery treat it.
H pylori (stomach ulcers) - treated by Prevpac.
139
Q

Patient with Mycobacterium Avium Complex, how do you treat?

A

Clarithromycin, Azythromycin, and Ethambutol.

140
Q

Patient with H. pylori, how do you treat?

A

Clarithromycin, Amoxicillin, Lansoprazole

141
Q

What treats Chlamydia trachomatis?

A

Azithromycin

Erythromycin

142
Q

What’s another use of erythromycin?

A

Stimulates motility of bowels; prokinetic effect.

143
Q

Why can’t you prescribe a Macrolide with a Class IA and III antiarrythmic?

A

QT segment is prolonged, causing Torsades de Pointes.

Can lead to cardiac arrest, because potassium channel is blocked and ventricles repolarize slower.

144
Q

What role to macrolides play when interacting with CYP enzymes?

A

Macrolide metabolites bind to CYP3A forming inactive complex. This INCREASES drug levels of CYP drugs (Digoxin, carbamasepine, cyclosporine, miazolam, theophylline, etc.).

145
Q

You get lab results and realize patient has high level of digoxin. You notice patient has been taking a macrolide for a URI. Whats your next move?

A

Macrolides inhibit the enzymes to metabolize digoxin; take patient off macrolide.

146
Q

MOA: Tetracyclines

A

Blocks translation by binding to ribosome.
Binds to rRNA to prevent tRNA from binding.

Bacteriostatic.

147
Q

Tetracycline, Minocycline, Doxycycline – Why is their coverage so important?

A

Atypicals, such as animal borne organisms, i.e. Yersinia pestis, Brucella Borrelia burgdorferi, rickettsiae.

Also do Enterococcus, MRSA, some GNeg and Anaerobes, T. pallidum, and H. Pylori.

NO MRSA or PSEUD.

148
Q

If your patient got a tick bite in the woods, how would you treat them?

A

Tetracyclines - treat borellia burgedorferi (Lyme disease tx)

149
Q

How would you treat Yersinia Pestis (the plague)?

A

Tetracyclines (covers atypicals).

150
Q

Your patient is an older woman with osteoporosis, why should you not prescribe her tetracyclines?

A

Depression of skeletal growth. Also, chelates with iron and calcium.

If you drink milk, medication won’t be absorbed and it’ll lead to treatment failure.

151
Q

What tetracycline treats chlamydia?

A

Doxycycline

152
Q

What is Glycylcycline?

A

Tigecycline (TYGACIL)

153
Q

MOA: Tygacil

A

Inhibits protein syntesis by binding to ribosome.

Bacteriostatic.

154
Q

Your patient has a skin infection caused by E. coli, MRSA, S. anginosus, S. pyogenes, and B. fragilis. What do you treat them with?

A

Tygacil

155
Q

Your patient has a complicated intra-abdominal infection caused by C. freundi, E coli, K. pneumoniae, E faecalis, MSSA, B. fragilis, etc. How do you treat?

A

Tygacil

156
Q

Whats the dosing consideration for Tygacil?

A

Hepatic dysfunction

157
Q

Tetracycline uses:

A

Tetracyclines also teat acne, pneumonia, Lyme Disease, Rocky Mt. Spotted Fever, and STDs.

158
Q

Bad people to prescribe tetracyclines to?

A

Under 8yo or pregnant females

159
Q

Dose adjustment for tetracyclines?

A

RENAL

160
Q

What doesn’t Tygacil cover?

A

VRE

161
Q

When is it ok to use Tygacil?

A

Last resort; used to prevent resistance.

162
Q

MOA of aminoglycosides?

A

Inhibition of protein synthesis

163
Q

Aminoglycosides

A

Amikacin
Gentamicin
Tobramycin

164
Q

Aminoglycoside coverage? Importance?

A

Gram negatives: pseudomonas, enterobacter, E. coli, Klebsiella pneumoniae, Proteus, Serratia.====SPACE BUGS.

Enterococcus when paired with PCN.***

165
Q

Aminoglycoside DOC for?

A

Febrile neutropenia, sepsis, enterococcus (synergy with PCN).

166
Q

Dosing considerations and adjustments of Aminoglycosides?

A

Renal toxicity, ototoxic, renal adjustment

REQUIRE THERAPEUTIC DRUG MONITORING

167
Q

Aminoglycosides - bacteriostatic or bactericidal?

A

Bactericidal

168
Q

Your pt has a high trough level on gentamycin, next course of action?

A

Extend dose until its under 1.

169
Q

Tobramycin level of 1.6, too high. Action?

A

Extend dose until its under 1.

170
Q

Oxazolinodinone

A

Linezolid

171
Q

What is Linezolid DOC for?

A

Note: Resistant gram positives finally are covered. MDR Pneumococcus, MRSA, and VRE.

DOC - HAP MRSA and CA MRSA

172
Q

Toxicity warnings for Linezolid?

A

Thrombocytopenia

Seratonin Syndrome

173
Q

MOA: Daptomycin

A

Bacterial depolarization whic inhibits DNA, RNA, and protein syntehsis

174
Q

Labs monitored on daptomycin?

A

CPK and pneumoniae.

175
Q

Why can’t daptomycin be used for a pneumoniae?

A

The surfactant deactivates it.

176
Q

MOA: Fluroquinolones

A

Inhibit DNA Gyrase and inhibit bacterial topoisomerase.

177
Q

Name the FQs.

A

Levofloxacin
Ciprofloxacin
Moxifloxacin

178
Q

Your pt has CAP, what FQ is not used for this?

A

Cipro; also not used for skin.

179
Q

If your pt has a UTI, which FQ would you not use?

A

Moxifloxacin

180
Q

What conditions are FQ’s used for?

A

Sinusitis, otitis, HAP at high doses, UTI, diarrhea, skin and osteomyelitis.

181
Q

Why can’t you drink dairy products with FQ?

A

They interact iwth iron, antacids, vitamins, calcium, and dairy.

182
Q

Why avoid a FQ to a cardiac patient? WHy not to elderly?

A

Risk of QT prolongation.

Warfarin interactions.

183
Q

Cipro

A

Gram negatives, atypical coverage, and pseud

184
Q

All FQ have renal dosing consideration, except:

A

Moxifloxacin, bc metabolized in liver.

185
Q

Levofloxacin

Moxifloxacin

A

CAP, Strep PNA and atypical coverage.

MOXI IS NOT USED FOR UTI.

186
Q

FQ ADR?

A 
Complexes with cations
Photosensitivity
Renal Elim
QT prolongation
Tendon rupture under eighteen years old
187
Q

Clindamycin

A

G+ and AN coverage

DOC for toxin mediated disease, i.e. TSS
Cellulitis
Osteomyelitis
Surgical prophylaxis for PCN allergy
INtraabdominal combination
188
Q

Clindamycin has a high risk of?

A

C. diff.

ALso neutropenia, thrombocytopenia, and pseudomembranous colitis.

189
Q

Sulfamethoxazole and Trimthoprim

A

Septra and Bactrim

190
Q

MOA: Septra and Bactrim

A

Inhibits conversion of PABA to DHF which inhibits folic acid use in the cell.

191
Q

What is a good prophylactic for AIDS, neutropenic, and chemo patients?

A

Septra and Bactrim.

192
Q

Clinical uses of Septra?

A

UTI, prostatitis, RTI, traveler’s diarrhea, shigella

193
Q

What three atypicals does septra cover?

A

Pneumocystis carinii, nocardia, toxoplasma gondii.

194
Q

Why shouldn’t you give Septra to a patient taking warfarin?

A

It will prolong INR time.

195
Q

MOA: Metronidazole

A

interacts with bacterial DNA to cause helical structure loss and strand breakage.

Bactericidal

196
Q

Metronidazole coverage?

A

Parasites, GPos, GNeg

197
Q

Metronidazole DOC?

A

C. Diff
Intra-abdominal combination
STI

198
Q

Why can’t you drink on motronidazole?

A

Dislfiram like reaction with ethanol.

199
Q

Polymixin B & E

A

MOA: Detergentlike mechanism allows for interaction with the LPS of outer membrane. DIsplaces mangesium and calcium disrupting the membrane = bactericidal.

Gram Negative coverage, but not used because of nephrotoxicity, neurotoxicity (paralytic).

200
Q

Why is there no resistance to Polymixin B & E?

A

Have not been used because of toxicity.

BLACKBOXED

201
Q

Rocephin - dosing consideration?

A

NO DOSE ADJ FOR RENAL INSUFFICENCY.

Clinical Pharmacology I (7 decks)

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