Antimicrobials Flashcards

1
Q

Should all surgical cases get an antibiotic?

A

No, you should weigh the risks and benefits. Is it worth exposing the patient to an antibiotic? For example, thyroid surgeries tend to NOT get infected. So you might hold off in this case.

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2
Q

What are the 3 general rules for using antibiotics in the surgical setting?

A
  1. You want to inhibit microorganisms as a level that is tolerated by the host. 2. In the seriously ill or immunocompromised you should use bactericidal as opposed to bacterostatic 3. Use a narrow spectrum before a broad spectrum to target a specific organism to preserve the patients normal flora.
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3
Q

When choosing an antibiotic for a patient is cost a factor?

A

Yes, providers need to choose cost effective antibiotics.

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4
Q

When choosing an antibiotic that seems cost effective, what is one thing you should consider?

A

Most of the cheaper antibiotics are broad spectrum. You must consider the benefit/risk of exposing the patient to a broad spectrum.

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5
Q

When should a surgical prophylactic antibiotic be given?

A

No more than 1 hour before incision, but completed before incision.

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6
Q

Are surgical prophylactic antibiotics a single-dose deal?

A

No, they can be continued for 48 hours in some cases.

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7
Q

Will giving a patient a brief course of antibiotics prophylactically increase resistance in organisms?

A

There is no evidence that a short course increases resistance.

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8
Q

When choosing an antibiotic for active infection, is it essential to identify the a causative organism?

A

Yes, so in this case, if there is an infected site that needs a washout or drained out, you may want to hold off on that first dose of antibiotic until after the intial incision is made and after samples for culture can be obtained.

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9
Q

Efficacy of antibiotic will depend on it’s _________ to the site of infection

A

delivery. Consider transport across blood brain barrier, if you have to deliver antibiotic to brain. Also, antibiotics will more readily penetrate infected tissue after it has been debrided and infectious material removed.

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10
Q

True or False. Using multiple antibiotics is the preferred method of treatment of infection.

A

False. Usually you treat with a single drug.

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11
Q

Does the route of administration need to be considered?

A

Yes. If it is orally administered it might suffer first pass metabolism and the complete dose will not reach the target tissue.

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12
Q

Does the duration of treatment need to be considered when choosing an antimicrobial?

A

Yes, is the patient going to have to take this medication at home?

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13
Q

What are the 2 main types of reactions that occur with antibiotics?

A
  1. Hypersensitivity 2. Direct drug toxicity
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14
Q

Does the dose of the antibiotic have anything to do with a hypersensitivity reaction?

A

No. It doesn’t matter what dose you gave, hypersensitivity can occur at even the smallest doses.

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15
Q

Does the antibiotic dose have anything to do with direct drug toxicity?

A

Yes. If you give more than can be cleared, the drug will reach toxic levels in the bloodstream.

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16
Q

What should you consider when giving antibiotics to a pregnant mother?

A
  1. most antimicrobials cross the placenta and enter breast milk. (Moms should discard milk for 24 hours) 2. We should be concerned with teratogenecity with any drug.
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17
Q

What are 4 physiological changes in the elderly that we need to consider when giving them antibiotics?

A
  1. They may have renal or liver impairment 2. They have decreased plasma proteins 3. Reduced gastric acid and motility 4. Increased body fat.
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18
Q

What would a decrease in plasma protein have to do with antibiotics?

A

If there are less plasma proteins for the medication to bind to then there is a higher free fraction of the drug in the bloodstream.

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19
Q

What is the difference between bactericidal and bacteristatic?

A

Bacterocidal drugs kill bacteria by disrupting cell wall synthesis. Bacteristatic drugs inhibit bacterial protein synthesis.

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20
Q

Is penicillin bactericidal or bacteristatic?

A

bactericidal

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21
Q

What family is pencillin part of?

A

the beta lactams

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22
Q

Which 3 main organisms does penicillin target?

A

pneumococcal, meningococcal, streptococcal.

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23
Q

How is PCN excreted?

A

90% of it is renally excreted

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24
Q

Name 2 derivatives of penicillin that we commonly see?

A

Ampicillin and Amoxicillin

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25
Q

Which has a wider range of activity, ampicillin or penicillin?

A

Ampicillin, it covers all the same stuff and penicillin plus some gram - like Haemophilus influenzae and E. Coli

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26
Q

Which is associated with a higher incidence of skin rash, ampicillin or amoxicillin?

A

ampicillin

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27
Q

Which is more effectively absorbed from the GI tract, ampicillin or amoxicillin?

A

amoxicillin

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28
Q

Which is more commonly used in pediatrics, amoxicillin or ampicillin?

A

Amoxicillin, because it can be given PO.

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29
Q

What is the most common adverse reaction to the pencillins?

A

hypersensitivity

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30
Q

Which is the most allergenic of all of the antibiotics?

A

Pencillin

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31
Q

What are 3 allergic type responses to penicillin?

A

Rash (with or without fever) anaphylaxis (immediate) and hemolytic anemia (this is rare)

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32
Q

What if a patient with with a penicillin allergy is ordered a cephalosporin?

A

There is an 8% chance of cross-sensitivity in patients with penicillin allergies who receive a cephalosporin. You may want to choose another drug, but at least you should give a test dose before administering

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33
Q

What do penicillin and cephalosporins have in common?

A

They have the same type of beta lactam ring

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34
Q

Are Cephalosporins bactericidal or bacterostatic?

A

bactericidal (damages cell wall synthesis)

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35
Q

Are cephalosporins broad or narrow spectrum?

A

broad

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36
Q

How are cephalosporins excreted?

A

Mainly by the kidney, but not as extensively as penicillin. 40% of a cephalosporin is excreted in the bile.

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37
Q

What is the most common allergic reaction to a cephalosporin?

A

rash

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38
Q

What percentage of patients receiving a cephalosporin have an anaphylactic reaction to it?

A

0.02% of treated patients

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39
Q

What 3 antibiotic types make up the beta lactam family and therefore could have cross-sensitivity reactions?

A

Penicillins, Cephalosporins, and Carbopenems

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40
Q

How many generations of cephalosporin antibiotics are there?

A

3

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41
Q

What is the difference between the generations of cephalosporins?

A

First generation are cheaper. As you move down to 3rd generation they get more effective against gram neg. bacteria.

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42
Q

Is Cefazolin a 1st, 2nd, or 3rd generation cephalosporin?

A

1st

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43
Q

Is cefoxitin a 1st, 2nd, or 3rd generation cephalosporin?

A

2nd

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44
Q

Is cefotaxime a 1st, 2nd, or 3rd generation cephalosporin?

A

3rd

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45
Q

Are cephalosporins ok to use in joint surgery?

A

Yes, the cephalosporins will all penetrate into joints.

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46
Q

Bacteriostatic agents ____________ the growth or replication of organisms but do not ________ the offending organism.

A

interfere with growth; do not kill

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47
Q

What is minimum inhibitory concentration?

A

the lowest concentration of a given antimicrobial at which an organisms growth is inhibited (this pertains to bacteriostatic agents)

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48
Q

Bactericidal agents _______ bacteria

A

kill

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49
Q

Are aminoglycosides bacteriostatic or bactericidal?

A

bactericidal

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50
Q

How does the bactericidal action of aminoglycosides work?

A

They destroy protein synthesis, but not at the cell wall, they enter the cell and destroy protein synthesis inside the cell, killing it.

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51
Q

Aminoglycosides are effective against ________ bacteria.

A

Gram negative

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52
Q

How are aminoglycosides excreted?

A

extensively excreted by the kidney

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53
Q

What is the elimination half-time of aminoglycosides?

A

2-3 hours

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54
Q

What happens to the elimination half time of aminoglycosides in patients with renal failure.

A

Increases 20-40 times! Watch the BUN/ Cr in these patients.

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55
Q

Name 3 side effects of aminoglycosides.

A
  1. ototoxicity 2.nephrotoxicity 3.skeletal muscle weakness
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56
Q

What effect do aminoglycosides have on neuromuscular blockade?

A

they prolong it

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57
Q

Is the ototoxicity associated with aminoglycosides dose dependent?

A

Yes, it is more likely to occur with chronic therapy

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58
Q

Describe the ototoxicity associated with aminoglycosides, what happens in the ear?

A

Vestibular/ auditory dysfunction occurs. There is drug-induced destruction of vestibular or cochlear sensory hairs. This can cause vertigo, ataxia, hearing loss, including complete deafness

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59
Q

Is the nephrotoxicity associated with aminoglycosides reversible?

A

Yes

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60
Q

Which aminoglycoside is the most nephrotoxic?

A

Neomycin

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61
Q

What is usually the first thing you will notice in aminoglycoside induced nephrotoxicity?

A

an inability to concentrate urine, watch that foley bag.

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62
Q

What are the changes you will see in the urine of a patient suffering from aminoglycoside induced nephrotoxicity?

A

inablity to concentrate urine, RBC casts in urine, and proteinuria

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63
Q

How exactly does the aminoglycoside induced nephrotoxicity damage the kidney?

A

Aminoglycoside accumulates in the renal cortex leading to tubular necrosis.

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64
Q

What happens to patients with mysasthenia gravis who get aminoglycosides?

A

Patients with myasthenia gravis are uniquely sensitive to the skeletal muscle weakness side effect associated with aminoglycosides.

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65
Q

If I have given my patient an aminoglyoside, and now I am ready to paralyze, would it matter if I used a depolarizing agent or a non-depolarizing agent to paralyze my patient?

A

No, it doesn’t matter, both will be affected by the aminoglycoside and can cause prolonged muscle weakness.

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66
Q

What happens at the neuromuscular junction in patients who have received an aminoglycoside and paralytic?

A

aminoglycosides can inhibit pre-junctional release of AcH and decrease post-synaptic sensitivity to the neurotransmitter.

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67
Q

True or False. A single dose of aminoglycoside in a healthy patient can cause problems.

A

False. It is usually not a problem.

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68
Q

Your patient getting a wound debridement has received a pre-op aminoglycoside, what else should you be aware of when giving a neuromuscular blocker?

A

Irrigation fluids used in wound debridement may have antibiotics in them, including aminoglycosides which could increase plasma concentrations of the drug. Remember… aminglycosides potentiate neuromuscular blockade.

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69
Q

At the end of the case, the neuromuscular blocker has worn off enough that your patient is breathing spontaneously again. They are ready to transfer to PACU, but they received an aminoglycoside during the case, what should you be aware of in PACU?

A

you can see an re-appearance of neuromuscular blockade in patients who have received aminoglycosides.

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70
Q

When lidocaine is used in cases where an aminoglycoside was given, what can happen?

A

the neuromuscular blocking properties of lidocaine will be enhanced.

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71
Q

rue rueIf my patient has been given an aminoglycoside, and I used a neuromuscular blocker, giving neostigmine will still work to reverse its effects. T or F.

A

False. neostigmine or calcium antagonism of neuromuscular blockade may be incomplete or transient in patients who have received aminoglycosides

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72
Q

If the train of 4 is normal, my patient is reversed and will not experience the side effect of aminoglycoside induced muscle weakness. T or F.

A

False. Even with a normal train of 4, my patient still may suffer prolonged muscle weakness.

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73
Q

Name 5 aminoglycosides.

A

Streptomycin and Kanamycin, Gentamicin, Amikacin, and Neomycin

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74
Q

Name this aminoglycoside. Used once to treat bubonic plague. Limited use now due to vestibular damage.

A

Streptomycin (or Kanamycin). Streptomycin specifically was used to treat plague.

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75
Q

Name this aminoglycoside. I am broader in spectrum that streptomycin. I am toxic at levels greater than 9 mcg/ml.

A

Gentamicin

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76
Q

Name this aminoglycoside. I am a derivative of kanamycin.

A

Amikacin

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77
Q

Name this aminoglycoside. I am used as adjunct therapy in hepatic coma to decrease ammonia levels. I am not usually given IV because of toxic effects. I used to be used routinely in burn dressings until my toxicity became an issue. I am one of the components of neosporin.

A

Neomycin

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78
Q

Are tetracyclines bacteriostatic or bactericidal?

A

Bacteriostatic (this is the brown stuff lining the central lines)

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79
Q

Because tetracylcines are bacteriostatic they kill bacteria. T or F

A

False. Bacteriostatic antibiotics don’t kill they just prevent protein synthesis.

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80
Q

Tetracycline decreases the fatty content in sebum and therefore is a good treatment for _________.

A

acne

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81
Q

How are tetracylcines excreted?

A

urine and bile

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82
Q

What are two main adverse reactions/ side effects associated with tetracyclines?

A

Photosensitivity and tooth discoloration

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83
Q

In what patient population does tooth discoloration from tetracyclines most commonly occur in?

A

children. you should also use caution in giving tetracycline to pregnant women, as the drug can cross the placenta and stain the baby’s teeth.

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84
Q

How exactly, does tetracycline stain the teeth?

A

It deposits in the teeth and bones forming tetracycline-orthophosphate-calcium complex

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85
Q

What is meant by phototoxicity related to tetracycline?

A

a sensitivity to sun and sunlight.

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86
Q

Is tetracycline given IV or PO?

A

PO only

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87
Q

Is doxycline given IV or PO?

A

either

88
Q

Which drug tetracyline or doxycycline, is the standard formulation?

A

tetracycline

89
Q

Which formulation, tetracycline or doxycycline is the long acting formulation?

A

doxycycline

90
Q

Name 2 common macrolides.

A

erythromycin and azithromycin

91
Q

Is erythromycin bacteriostatic or bactericidal?

A

It can be either, depending on what environment it is in.

92
Q

Is erythromycin broad spectrum or narrow spectrum?

A

narrow

93
Q

What organisms does erythromycin cover?

A

Mostly gram positive bacteria

94
Q

How is erythromycin metabolized?

A

By the liver. It is metabolized by the cytochrome P-450 system and excreted mostly in the bile.

95
Q

True or False. You must use caution when giving macrolide antibiotics to patients in renal failure.

A

False, macrolides are metabolized by the liver, they do not need to be renally adjusted.

96
Q

Name 4 adverse reactions of macrolides.

A
  1. GI intolerance 2.Gastric emptying 3. QT effects 4.Thrombophlebitis
97
Q

What is the most common side effect of macrolides?

A

Gi intolerance

98
Q

Which GI side effect can tends to occur with IV infusion of macrolides?

A

Severe N/V, cramping

99
Q

Which QT effects have been reported with macrolide use?

A

prolonged cardiac repolarization. Reports of torsades de pointes

100
Q

When using macrolides IV for a prolonged period of time, your patient is increased risk of:

A

thrombophlebitis

101
Q

How do anitepileptics affect the cytochrome P-450 system?

A

They usually increase its activity and it will metabolize drugs quicker than normal. However, the opposite has also occured.

102
Q

Which class of antibiotics does clindamycin belong to?

A

Linomycins

103
Q

Is clindamycin bacteriostatic or bactericidal?

A

bacteriostatic

104
Q

Which drug is clindamycin similar to in antibiotic activity?

A

erythromycin

105
Q

Clindamycin is more active than erythromycin against ___________.

A

anaerobes

106
Q

Which antibiotic is good for serious infections of the GI tract or female genital tract?

A

Clindamycin

107
Q

You need to be cautious using clindamycin in patients with:

A

severe liver disease; you’ll want to decrease the dose.

108
Q

What is one major GI complication associated with clindamycin?

A

pseudomembranous colitis. It causes severe diarrhea.

109
Q

If your patient on clindamycin presents with pseudomembranous colitis, what do you do to treat it?

A

stop antibiotics immediately.

110
Q

What is pseudomembranous colitis?

A

severe antibiotic associated diarrhea caused by an imbalance in the normal intestinal flora. It is not necessarily a c.diff infection. Nonetheless, clindamycin must be stopped. The treatment for diarrhea is usually vanco and flagyl.

111
Q

Does clindamycin cause any problems with neuromuscular blockers?

A

Yes. It affects both the pre and post junction cells. It will cause the blocker to not be metabolized with anticholinesterases or calcium. If you give large doses, you can cause long lasting, profound neuromuscular blockade.

112
Q

Can clindamycin cause muscle relaxation on its own or is it only when it is given in conjunction with a neuromuscular blocker?

A

It can cause muscle relaxation on its own.

113
Q

What type of drug is vancomycin?

A

It is a glycoprotein derivative

114
Q

Is vancomycin bacteriostatic or bactericidal?

A

bactericidal

115
Q

What organisms does vancomycin target?

A

Gram + organisms.

116
Q

What sorts of infections would you use vancomycin to treat?

A

severe staph infections, streptococcal or enterococcal endocardidits, MRSA, and in patients with penicillin and cephalosporin allergies.

117
Q

How is vancomycin excreted?

A

Renally.

118
Q

What is the elimination half time of vancomycin?

A

6 hours, but can last up to 9 days in patients with renal failure.

119
Q

Name 3 common cases in which vancomycin is given.

A

Cardiac procedures, orthopedic procedures using prosthetic devices, CSF and shunt infections.

120
Q

What is the typical dose of vancomycin?

A

10-15mg/kg over 60 minutes. 1 gram mixed in 250 mL.

121
Q

How quickly can you administer vancomycin?

A

It should be given over at least one hour.

122
Q

If you give vancomycin too quickly a serious cardiovascular complication can occur, what is it?

A

Profound hypotension due to histamine release.

123
Q

Why is there a histamine release with vancomycin?

A

Vancomycin has a direct toxic effect on mast cells.

124
Q

What is ‘red man’ syndrome?

A

Intense facial and truncal erythema from histamine release.

125
Q

How can you prevent red man syndrome?

A

Give the infusion slower.

126
Q

Does giving vancomycin slower always prevent red man syndrome?

A

No

127
Q

What are 2 major adverse reactions that can occur with vancomycin?

A

ototoxicity and nephrotoxicity

128
Q

Is there any risk of a return of neuromuscular blockade with vancomycin?

A

Yes, but Ms. Tolla has never seen this in her practice.

129
Q

Are sulfonamides bacteriostatic or bactericidal?

A

bacteriostatic.

130
Q

How do sulfa drugs work?

A

They inhibit the enzyme DHPS (dihydropteroate synthase) from synthesizing folate, an essential nutrient for bacteria.

131
Q

Name a common use for sulfonamides?

A

To treat urinary tract infections

132
Q

How are sulfonamides metabolized?

A

Metabolized by the liver and excreted by the kidney.

133
Q

Name 4 side effects of sulfonamides?

A
  1. anywhere from skin rash to anyphylaxis 2. drug fever 3. hepatotoxicity 4.acute hemolytic anemia
134
Q

Do sulfanomides have any effect on anticoagulants?

A

Yes, they increase the effect of PO anticoagulants like coumadin

135
Q

Are polymyxin B and E bacteriostatic or bactericidal?

A

Bactericidal. They affect bacterial wall membrane phospholipids.

136
Q

What is the trade name for polymyxin E?

A

colistin, colistemethate

137
Q

What organisms are targetted by polymyxin B and E?

A

Gram negatives.

138
Q

What sorts of infections would you treat with Polymyxin B and E?

A

Severe UTIs, infection of skin, mucus membranes, eyes and ears.

139
Q

How are polymyxin B and E eliminated by the body?

A

via the kidney

140
Q

Can patients with renal failure take polymyxin B or E?

A

Yes, but these drugs accumulate in patients with renal failure.

141
Q

Which antibiotics have the most potent effects at the neuromuscular junction?

A

Polymyxin B and E

142
Q

Do polymyxin B and E affect the presynaptic junction or the post?

A

presynaptic

143
Q

How severe is the muscle weakness that can occur with polymyxin B and E?

A

It can produce skeletal muscle weakness resembling non-depolarizing neuromuscular blockade

144
Q

What happens to neuromuscular blocking agents when combined with polymyxin B and E?

A

there is marked potentiation of the neuromuscular blocker.

145
Q

Will neostigmine and calcium work to antagonize a neuromuscular blocking agent once polymyxin B or E has been given?

A

not reliably

146
Q

Do polymyxin B and E affect the kidneys?

A

Yes, they are highly nephrotoxic and neurotoxic

147
Q

Is metronidazole a bacteriostatic or bactericidal agent?

A

Bactericidal

148
Q

What organisms are targetted by metronidazole?

A

Anaerobic Gram negative bacilli

149
Q

What sorts of infections does metronidazole treat?

A

A wide variety, CNS, abdominal and pelvic infections, and pseudomembranous colitis

150
Q

Are fluroquinolones broad spectrum or narrow spectrum?

A

broad

151
Q

Are fluroquinolones bacteriostatic or bactericidal?

A

bactericidal

152
Q

What type of bacteria do fluroquinolones treat?

A

enteric gram negative bacilli

153
Q

What is the elimination half time of fluroquinolones?

A

3-8 hours

154
Q

How are fluroquinolones metabolized?

A

By the P-450 system; however, fluroquinolones can inhibit P-450 enzymes

155
Q

How are fluroquinolones excreted?

A

mostly renal, through glomerular filtration and renal tubular secretion.

156
Q

Do you need to consider renal function when giving fluroquinolones?

A

Yes. you must decrease the dose in a patient with impaired renal function.

157
Q

Name 2 popular fluroquinolone drugs?

A

Cipro and levaquin

158
Q

Are there any GI side effects from fluroquinolones?

A

only mild GI disturbances

159
Q

For complicated GI and GU infections, which group of antibiotics is very effective?

A

The fluroquinolones

160
Q

Ciprofloxacin is commonly used to treat:

A

a variety of systemic infections including bone, soft tissue, and respiratory tract.

161
Q

Name the antibiotic commonly used to treat tuberculosis.

A

Rifampin

162
Q

Is rifampin bacteriostatic or bactericidal?

A

It is bactericidal for mycobacteria.

163
Q

How does rifampin kill mycobacteria?

A

It acts on their DNA and RNA

164
Q

Does rifampin work on Gram negative or Gram positive bacteria in addition to mycobacteria?

A

Yes, it inhibits growth of most gram positive and gram negative bacteria.

165
Q

Does rifampin cross to the CNS?

A

Yes, it’s fat solubility allows it to cross into the CNS and penetrate tissues

166
Q

Is rifampin given by oral or parenteral route?

A

either

167
Q

How is rifampin excreted?

A

in bile and urine

168
Q

What is one unfortunate complication of rifampin?

A

It develops resistance pretty quickly

169
Q

Are side effects common with rifampin therapy?

A

No

170
Q

If side effects do occur with rifampin, what are they?

A

Typically seen in higher doses. Thrombocytopenia, anemia, hepatitis, fatigue, numbness, and skeletal muscle weakness.

171
Q

Does rifampin have any effect on the cytochrome P-450 system?

A

Yes! rifampin is a potent inducer of the P-450 system which will accelerate the metabolism of opioids, neruomuscular blocking agents, and warfarin.

172
Q

What laboratory testing should be done before beginning therapy with rifampin?

A

LFTs.

173
Q

What sort of drug is amphoterecin B?

A

antifungal

174
Q

Amphotericin B is used to treat for:

A

yeasts and fungus

175
Q

Can amphoterecin B be given orally?

A

No, there is poor PO absorption. Amphoterecin B is given IV

176
Q

How is amphoterecin B excreted?

A

Renally

177
Q

Why is amphoterecin B such a nasty drug?

A

It compromises renal function in 80% of the patients that take it. Most recover after drug is stopped but some resulting permanent decrease in glomerular filtration rate may remain.

178
Q

What lab value must be monitored in patients receiving amphoterecin B?

A

plasma creatinine

179
Q

Amphoterecin must be given by slow infusion because ______, ________, ________, and ________ can occur during infusion.

A

fever, chills, dyspnea, and hypotension

180
Q

Name 6 potential side effects of amphoterecin B.

A

impaired hepatic function, hypokalemia, allergic reactions, seizure, anemia, thrombocytopenia

181
Q

Viruses are really intracellular _________.

A

parasites.

182
Q

Can viruses reproduce outside of the host cell?

A

No

183
Q

Viruses use many of the _________________ of the host cell.

A

biochemical mechanisms

184
Q

True or False. Development of antivirals is difficult.

A

True

185
Q

One way to combat viruses is to:

A

vaccinate

186
Q

Name 4 common vaccines for viruses.

A

HPV, Hepatitis A and B, Herpes Zoster (shingles)

187
Q

Viruses are composed of:

A

a nucleic acid core surrounded by a protein containing outer coat.

188
Q

Viruses contain ____ or ___ but never both.

A

DNA or RNA

189
Q

How are antivirals classified?

A

By whether the virus they kill has a genome with DNA or with RNA

190
Q

Name 2 antivirals used to treat herpes viruses.

A

Acyclovir and Valacyclovir

191
Q

How are acyclovir and valacyclovir excreted?

A

by the kidneys

192
Q

What is vidarabine used to treat?

A

An antiviral used to treat cytomegalic inclusion disease and herpes simplex encephalitis

193
Q

What is one major concern with vidarabine?

A

It can be mutagenic and carcinogenic

194
Q

What is famcilovir for?

A

It is an antiviral used to treat acute herpes zoster

195
Q

What is ganciclovir used for?

A

It is an antiviral used to treat cytomegalovirus

196
Q

Name one adverse event associated with ganciclovir.

A

Hematologic toxicity (bone marrow suppression)

197
Q

What is amantadine used for?

A

An antiviral used to treat influenza A

198
Q

How is amantadine excreted?

A

renally

199
Q

What is an interferon?

A

A glycoprotein produced in response to a viral infection.

200
Q

Do our bodies produce interferons?

A

yes, they boost our body’s ability to fight infections.

201
Q

How do interferons work?

A

They bind to receptors on host cell membranes and induce the production of enzymes that inhibit viral replication this leads to the degradation of viral mRNA

202
Q

Does interferon have any effect on macrophages?

A

Yes, they enhance the tumoricidal activities of macrophages.

203
Q

Interferons are commonly used to treat:

A

chronic Hepatitis B, Hepatitis C, and rhinovirus (interferon in the form of nasal sprays)

204
Q

What are some of the CNS effects of interferon?

A

It can cause depression and irritability, and decreased mental concentration

205
Q

Can interferon affect your blood?

A

Yes, inteferon can cause hematologic toxicity (bone marrow suppression)

206
Q

Does intereferon affect CV, thyoid, hepatic functions?

A

Yes

207
Q

What are some of the other side effects of interferon?

A

It can cause flu-like symptoms and autoimmune conditions. It can also cause rash. skin eruptions and alopecia

208
Q

What are the 3 main classes of antivirals for HIV/AIDs?

A

NRTIs (nucleoside reverse transcriptase inhibitors), NNRTIs (nonnucleoside reverse transciptase inhibitors), and protease inhibitors

209
Q

How do NRTIs work?

A

NRTIs act as an imposter cell, so the HIV virus incorporates into the fake cell and can no longer elongate or replicate

210
Q

How do NNRTIs work?

A

they inhibit the function of an enzyme used by the virus, this prevents replication and division.

211
Q

How to protease inhibitors work?

A

they bind to HIV protease and inhibit replication and division

212
Q

Which one antiviral is used to treat HIV/ AIDS

A

not one alone, most commonly HIV/ AIDS is treated with a combination therapy

213
Q

Name some of the many and varied side effects of the antivirals used for HIV/AIDS.

A

Pancreatitis, hepatotoxicity, lactic acidosis, fat redistribution, increases in serum cholesterol and triglycerides, and hypersensitivity

214
Q

Do protease inhibitors affect the P-450 system?

A

Yes, most of them inhibit the P-450 system

215
Q

Which of the protease inhibitors is the most potent inhibitor of the P-450 system?

A

Ritonavir

216
Q

Because protease inhibitors inhibit the P-450 system, what happens to drug concentrations in the body?

A

We will see large plasma increases of many drugs including analgesics, lidocaine, antimicrobials, anticonvulsants, anticoagulants, antiemetics, and calcium channel blockers.