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MOD Exam III - Antibiotics > Antibiotics (Sheehy) > Flashcards

Antibiotics (Sheehy) Flashcards

1
Q

What is the structure of Penicillins made of?

A

Thiazolidine Ring Beta Lactam Ring

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2
Q

How Do Penicillins kill bacteria?

A

Interfere with Transpeptidation Rxn

Inhibit Cell Wall Synthesis

(MUST BE ACTIVELY GROWING)

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3
Q

How are Penicillins rendered inactive?

A

Beta Lactamases

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4
Q

How are Pencillins able to kill Gram-Negative Bacteria?

A

They enter them through Porins

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5
Q

What are the (3) methods of Penicillin Resistance?

A

1) Altering Porin Channels
2) Altering structure of Pencilin Binding Protein
3) Increasing efflux of penicillin out

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6
Q

What is the Original Penicillin?

A

Penicillin G

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7
Q

What is Penicillin G able to kill?

A

S. Pneumonia

S Pyogenes

S Viridans

N Meninigitids

Spirochetes (T Pallidum, C. Perferingens)

(BEST AGAINST GRAM POSITIVES, GRAM NEGATIVE COCCI, AND NON-BETA LACTAMASE PRODUCING ANEAROBES)

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8
Q

What is a key adverse effect to taking Penicillins?

A

Hypersensitivty to Beta Lactam Ring

– life threatening anaphylaxis

– GI Symptoms - N/V/D

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9
Q

What are the Aminopenicillins?

A

Ampicillin, Amoxicillin

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10
Q

How do we normally make aminopenicillins more effective?

A

By combining them with Beta Lactamase Inhibitors

(IE: Amoxicilin Clauvulinic Acid) 850-150 mg

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11
Q

What do Aminopenicillins kill?

(What about with Beta Lactamase inhibitors?)

A

Gram Positives

Some Gram Negatives: E Coli, Enterics (Proteus, Salmonella, Shigella)

[with the combo of beta lactamase inhibitors)

H Influenzae

E Coli

Klebsiella spp

Proteus spp

B Fragilis

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12
Q

What are the drugs of Pencillinase Resistant Pencillins?

A

Nafcillin, Oxacillin, Dicloxacillin (Methicillin – but not in US)

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13
Q

How are drugs like Nafcillin, Oxacillin, Dicloacillin better than the previous Pencillins?

A

They have decreased susceptibility to Beta Lactamase

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14
Q

All Pencillins are:

A

Bactericidal

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15
Q

What do Pencillinase Resistant Pencillins kill?

What are they Resistant too?

A

S. Aureus

S Epidermidis (have poor gram positive coverage)

Resistant to MRSA and MRSE

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16
Q

What are the Antipseudomonal Penicillins?

A

Piperacillin (a uriedopenicillin – no carboxypenicilins are in the US)

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17
Q

What are Antipseudomonal Penicillins good for?

A

Targeting P. Aeurginosa - most effective against dividing bacteria

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18
Q

What is Piperacillin (a Antipseudomonal Penicillin) combined with?

A

Tazobactam (Beta Lactamase inhibitor)

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19
Q

What does the combo Penicillin Piperacillin/Tazobactam target?

A

P Aeuroginosa

S Aureus

Enterococcus faecalis

Klebsiella Pneumonia

E Coli

H Influenzae

B Fragilis

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20
Q

Which Penicillin has the broadest spectrum of all Penicillins?

A

Piperacillin (Antipseudomonal Penicillin)

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21
Q

How do Cephalosporins kill bacteria?

A

Cell Wall Inhibitor

Inactivate Transpeptidase

Best in Rapidly Proliferating Bacteria

Bactericidal

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22
Q

What is the base structure of Cephalosporins?

A

7-aminocephalosporanic acid (very similar to penicillin)

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23
Q

Main ways bacteria have evaded Cephalosporins?

A

Altering Porins

Altering structure of transpeptidase

Increase Efflux Pumps

Beta Lactamases (IE: Klebsiella and E Coli)

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24
Q

What is the general rule of the generations of Cephalosporins?

A

1st Gen – good against Gram +

3rd Gen – good against Gram -

2nd Gen – Ok against both +/-

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25
Q

What is the main Hypersensitivity for Cephalosporins?

A

to the Beta Lactam Ring – with a Maculopapular rash that develops several days after therapy.

(accompanied with Eosinophilia and Fever)

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26
Q

What are the 1st Gen Cephalosporins?

A

Cefazolin

Cephalexin

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27
Q

What are the 1st gen Cephalosporins active against?

A

(INJUSTICE) . . . actually

S Aurues and most Gram + (VERY GOOD)

Moraxella Catarhallis, K Pneuomonia, E Coli, Proteus Mirabilis (OK)

NOT: MRSA, Enterococci, S Epidermidis, B Fragilis

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28
Q

What are the 2nd Gen Cephalosporins?

(What subclass is also in this group?)

A

Cefurixome

Cefaclor

Cefprozil

Cefamycins – Cefotetan, Cefoxitin

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29
Q

What do the 2nd Gen Cephalosporins Kill?

A

Expanded Gram Neg Coverage

– including Klebsiella, H Influenzae, N Meningitidis, S Pneumoniae

NOT: Serratia, B Fragilis

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30
Q

What do the Cephamycins kill?

A

B Fragilis

Serratia

NOT: H Influenzae

[Cephamycins are resistant to Beta Lactamases]

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31
Q

What do 2nd Gen Cephalosporins NOT cover?

A

NO Coverage of: Enterococci

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32
Q

Cefotetan (a Cephamycin) has what adverse effect?

A

Hypoprothrombinemia and bleeding due to the methylthiotetrazole group on its structure

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33
Q

What should you never take with Cefotetan?

A

Alcohol

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34
Q

What are the 3rd Generation Cephalosporins?

A

Cefotaxime, Cefixime, Cefdnir, Ceftibuten, Ceftazdime, Ceftriaxone, Cefpodoxime Proxetil, Cefditoren Pivoxil

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35
Q

What are the 3rd Gen Cephalosporins active against?

A

(JUSTICE) . . . no? too much?

Neisseria spp, Haemophilus spp,

NOT: Enterobacter spp (anything that has consitutive expression of beta lactase)

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36
Q

What is the only 3rd Gen Cephalosporins that is active against P Aeruginosa?

A

Ceftazidime

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37
Q

What are the 2 prodrugs in the 3rd Ceph family?

A

Cefpodoxime Proxetil and Cefditoren Pivoxil – hydrolyzed to active forms

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38
Q

Cefixime, Cefpodoxime Proxetil, Cefdinir, Ceftibuten are active against what?

A

E Coli

H Influenzae

P Mirabilis

S Pyogenes

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39
Q

Ceftriaxone may cause what?

A

Jaundice in Neonates

Gall Stones (Biliary Pseudolithiasis)

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40
Q

What are the 4th Gen Cephalosporins?

A

Cefepime

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41
Q

What are the 4th Gen Cephalosporins active against?

A

. . . . you wanted me to say it. . . .

Enterobacter, Pseudomonas

BAD: B Fragilis

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42
Q

What are the 5th Gen Cephalosporins?

A

Ceftaroline Fosamil

Ceftolozane (usually with Tazobactam)

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43
Q

The 5th Gen Cephalosporins are good against?

A

MRSA, Pseudomonas, S. Pneumoniae

NOT: B Fragilis

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44
Q

What are the Carbapenems?

A

Ertapenem

Meropenem

Doripenem

Imipenem

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45
Q

How do Carbapenems work?

A

(by working duh . . .)

Inhibiting Transpeptidase, Inhibiting Cell Wall (decreasing cross linking), Resistant to Beta Lactamases

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46
Q

How do Bacteria resist Carbapenems?

A

by “Carbon” loading them with so much food?!?! (No you silly goose)

Shrink Down Porin Channels

Upreg of Carbapenemases

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47
Q

What are Carbapenems good against?

A

Gram Neg Bacteria

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48
Q

Imipenem (a Carbapenem) is active against what?

A

(Its WIDE SPECTRUM) Gram Positives Anaerobes Most Gram Neg Rods (with P Aeruginosa)

IE: Listera, Staphylococci (including MRSA) Enterococci (NOT: Enterococcus Faecium) Streptococci (including Penicillin resistant S Pneumoniae) Enterobacteriacae, Acinetobacter spp, B Fragilis

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49
Q

What Bacteria are resistant to Imipenem (a Carbapenem)?

A

Stenotrophomonas Maltophillia

Burkholderia Cepacia

Clostridium Difficile

MRSA (some strains)

Enterococcus Faecium

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50
Q

Doripenem and Meropenem (Carbapenems) are more active against what?

A

Gram Neg

(less active with Gram Positives IE: Enterococcus)

They are also not degraded by Renal Dipeptidase Enzymes

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51
Q

Ertapenem (a Carbapenem) is not active against what?

A

P Aeruginosa

Acinetobacter spp (less active against Enterococcus)

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52
Q

What are the adverse effects of Imipenem use? (a Carbapenem)

A

Skin Rash

Diarrhea

Vomiting

Nausea

Renal Failure, Seizures (at high levels of the drug)

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53
Q

What is the structure of the Monobactams?

A

they have a Monolithic Beta Lactam Ring

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54
Q

What is the Monobactams that we need to know?

A

Aztreonam

55
Q

What does Aztreonam (a Monobactam) inhibit?

A

It inhibits the gram-negative specific subtype of the transpeptidase enzyme –> Bacterial cell wall loses rigidity –> bacteria dies

56
Q

Is Aztreonam susceptible to Beta Lactamases?

A

YES! It still has a Beta Lactam ring

57
Q

What does Aztreonam (Monobactam) have no activity against?

A

No activity against Gram Positives or Anaerobes

58
Q

What does Aztreonam have activity against?

A

(only Gram Negs, and Aerobes) Enterobacteriaceae and P. Aeruginosa, H Influenza (A lot like Ceftazidime – 3rd gen cephalosporin)

59
Q

What patients can take Aztreonam?

A

Penicillin Allergic patients (beta lactamase allergic people can take this drug) Sometimes skin rashes occur but not often

60
Q

What are the main Glycopeptides? What are the main Lipoglycopeptides?

A

Glyco: Vancomycin

Lipo: Telavancin, Dalbavancin, Oritavancin

61
Q

How do Glycopeptides and Lipoglycopeptides work?

A

By being Cell wall synthesis inhibitors

  • They bind to D-Alanyl-D-Alanine terminus with high affinity
  • they inhibit transglycosylase

– no cross linking of peptidoglycans Lipoglyco- improve on this and dimerize and embed their lipid structures in to the cell wall. (Increases Potency)

62
Q

What do Oritavancin and Telavancin (Lipoglycopeptides) do specifically?

A

Disrupt the bacterial membrane allowing them to have a more rapid bactericidal effect

63
Q

What species are resistant to Glycopeptides?

A

Enterococci spp (esp – E Faecium) Resistance is on a transposon – so its scary!

64
Q

Vancomycin (a Glycopeptide) is active against what?

A

Gram + like: Ampicillin Resistant Enterococci, Penicillin Resistant Streptococci, MRSA

65
Q

What bacteria are resistant to Vancomycin (a Glycopeptide)

A

Erysipelothrix, Leuconostoc, Pediococcus, Lactobacillus ALL GRAM NEG Bacilli and Mycobacteria are resistant

66
Q

Can Lipoglycopeptides and Glycopeptides go through porins?

A

NO! They are too big to penetrate the outer membrane of Gram Neg

67
Q

How can Vancomycin be effective systemically?

A

Give it in an IV, not orally

68
Q

What are the Key Adverse effects of Lipoglycopeptides and Glycopeptides?

A

Red Man Syndrome – Hypotension, Tachycardia, and flushing

THIS IS NOT AN ALLERGY – its just a interaction with mast cells

Nephrotoxicity is another more serious issue

69
Q

What are the Beta Lactamase Inhibitors?

A

Clauvulinic Acid

Sulbactam

Tazobactam

70
Q

What do you do with Beta Lactamase Inhibitors?

A

You pair them with other antibacterial (because they are weak alone) and not all are inhibited by beta lactamases) Very few adverse effects – look to the main drug for problems

71
Q

Beta Lactamase Inhibitors extend coverage for what main bacteria?

A

Aminopenicillin attacks on: H Influenzae, E Coli, Klebsiella, Proteus, B Fragilis

72
Q

What are the Oxazolidinones?

A

Linezolid

Tedizolid

73
Q

What do Oxazolidinones act mainly against?

A

Gram Positive Bacteria

Enterococci, Streptococci, Staphylcocci,

Gram + anaerobic cocci, L Monocytogenes, Corneybacterium spp, Nocardia spp, Good for Resistant strains: MRSA, penicillin resistant S pneumoniae

(POOR COVERAGE of Gram -)

74
Q

How do Oxazolidinones act against bacteria?

A

Bind to the P site on the 50S ribosome, and prevent the formation of the fMet tRNA complex. (they are Bacteriostatic, but are Bactericidal against Streptococci)

75
Q

How do bacteria become resistant to Oxazolidinones?

A

Point mutations on the 23S rRNA (takes mutations on two or more 23S rRNAs) A Methyltransferase that can modify the Ribosome and alter binding (this is transferable between bacteria – BAD)

76
Q

What are the 3 different categories of Adverse effects of Oxazolidinones?

A

Myelosuppression

Mitochondrial Toxicity

Drug-Drug Interactions

77
Q

Explain Myelosuppression of Oxazolidinones?

A

Most commonly Thrombocytopenia (Tenzolid may have less of this problem)

78
Q

Explain Mitochondrial Toxicity of Oxazolidinones?

A

Lactic Acidosis, Optic Neuritis, Peripheral Neuropathy can develop in patients taking Linezolid. Linezolid should not be used for Long Term Treatment

79
Q

Explain Drug-Drug Interactions of Oxazolidinones?

A

Linezolid is a weak inhibitor of MAO – this causes interactions with SSRIs – can lead to serotonin syndrome

80
Q

What is Serotonin Syndrome with taking Oxazolidinones?

A

Life Threatening, can manifest as Headaches, palpitations, and hypertensive crisis.

81
Q

What are the main Macrolides and Ketolides to know?

A

Macrolides: Erythromycin, Clarithromycin, Azithromycin, Fidaxomicin Ketolide: Telithromycin

82
Q

What is Fidaxomicin (a Macrolide) used to treat?

A

C Difficile colitis

83
Q

How do Macrolides and Ketolides kill bacteria?

A
  • Protein Synthesis Inhibitors Bind reversibly to 50S ribosomal subunit prevents translocation of tRNA from the A site to the P site
  • Elicit Conformational change in Bacterial ribosome this can indirectly inhibit transpeptidation

(BOTH Macrolides and Ketolides are Bacteriostatic)

84
Q

What are the 4 main mechanisms of resistance to Macrolides and Ketolides?

A

1) Active Drug Efflux
2) Ribosome is shielded or protected from them (by Methylase enzymes)
3) Degradation of the drug
4) Mutations to the 50S subunit can occur

85
Q

Erythromycin (a Macrolide) has good activity against what?

(warning: its a hefty amount)

(I don’t blame you for skipping past this card – I will too)

A

Erythromycin has good activity against streptococci, pneumococci, staphylococci. In addition, erythromycin is active against: C. jejuni, M. pneumoniae, Legionella pneumophila, C. trachomatis, Chlamydophila psittaci, Chlamydophila pneumoniae, H. pylori and the gram-positive bacilli including Clostridium perfringens, Corynebacterium diphtheriae, and L. monocytogenes. Some gram-negatives are also susceptible to erythromycin and these include Bartonella spp., Quintana spp., Neisseria spp., Rickettsia spp., and Treponema pallidum.

(I don’t blame you for skipping past this card – I will too)

86
Q

What are Erythromycin (a Macrolide) not good against?

A

Mean words spoken about them by other antibiotics — noooo

Most Aerobic Enteric Gram Neg Bacilli

87
Q

What is Azithromycin (a Macrolide) active against?

A

Azithromycin is active against Moraxella catarrhalis, Chlamydia spp. (highly active), L. pneumophila, B. burgdorferi, M. pneumoniae, and H. pylori. Azithromycin is less active than erythromycin and clarithromycin against streptococci and staphylococci.In contrast, azithromycin is more active against H. influenzae.

88
Q

What is Clarithromycin (a Macrolide) active against?

A

Clarithromycin is more potent than erythromycin against sensitive streptococci and staphylococci. In addition, clarithromycin is active against same bacteria highlighted with azithromycin. Like azithromycin, Clarithromycin is also active against H. influenzae.

89
Q

What is Fidaxomycin (a Macrolide) active against? (don’t skip this one — its short)

A

C Difficile (in GI Tract)

90
Q

What is Telithromycin (a Ketolide) active against?

A

similar to azithromycin and clarithromycin but with better attacking power of S Pneuominae and S Aureus Macrolide resistant strains

91
Q

What are the most common adverse affects of Macrolids and Ketolides?

A

Diarrhea, Nausea, Vomiting, and Anorexia Hepatotoxicity (with prolonged Eryhthromycin, Clarithromycin and Azithromycin use)

92
Q

What are the signs of hypersensitivity to Macrolides and Ketolides?

A

Skin Eruptions, Eosinophilia, and Fever

93
Q

What are the main drugs of Streptogramins? (and their percentages?)

A

Streptogramin A –> Dalfopristin (70%)

Streptogramin B –> Quinupristin (30%)

always are in a combined ratio

94
Q

How do Streptogramins attack bacteria?

A

Inhibit Protein Synthesis by binding to 50S Ribosomal subunit Quinupristin

– inhibits polypeptide elongation/early term of protein Dalfopristin

– binds to nearby site, causing conformational change // impedes polyp chain formation

95
Q

How do Bacteria cause resistance to Streptogramins? (3)

A

1) Enzymatic inactivation of Dalfopristin (Strepto A)
2) Binding site of Quinipristin can be altered (Strepto B)
3) Both can be subjected to efflux

96
Q

What are Streptogramins active/and not active against?

A

NOT active against GRAM NEG Bacteria Active against: gram positive cocci including resistant streptococci, penicillin-resistant S. pneumoniae, and methicillin resistant staphylococci. In addition, quinupristin/dalfopristin is active against M. pneumoniae, C. pneumoniae, and Legionella spp.

97
Q

What are the problems associated with taking Streptogramins?

A

Infusion site reactions – with pain and arthralgia-myalgia syndrome

98
Q

What are the main Tetracylcines and Glycylcyclines?

A

Tetracyclines: Doxycycline, Tetracycline, Minocycline, Demeclocycline

Glycycyclines: Tigecycline

99
Q

How do Tetra and Glycylcyclines attack bacteria?

A

Protein synthesis inhibitors Bind the the 30S ribosomal subunit - prevent tRNA from binding to the A site

100
Q

How do Bacteria make resistance to Tetra and Glycylcyclines?

A

1) Reduced Intracellular Concentration

a – energy dependent efflux path

b – glycyclines are able to overcome tetracycline resistance by these efflux pumps

2) Upreg of a protein that dislodges them from their target
3) Inactivated enzymatically

101
Q

What do Tetracyclines attack? (this is a lot, just know the 1 spirochete and generals of the other)

A

GOOD: Gram +, Anaerobes: IE: Chlamydiae, Mycoplasmas, Rickettsiae (MRSA), Streptococcus pyogenes, Streptococcus pneumoniae, Bacillus anthracis, Listeria monocytogenes, Haemophilus influenzae, Vibrio cholera, and Helicobacter pylori. Ureaplasma spp., Coxiella burnetii, Mycoplasma pneumoniae, Rickettsia spp., Chlamydia spp., Legionella spp., and Plasmodium spp. and 1 spirochete: T Pallidum

102
Q

What are Tetracyclines not good against?

A

Inactive against: Pseudomonas, Proteus, Providencia

103
Q

What do Glycylcyclines attack?

A

same as tetracycline, but with added activity against bacteria resistant to tetracyclines Tigecycline has much greater activity against enterococci, enterobacteriaceae, Acinetobacter spp., and B. fragilis. Pseudomonas, Proteus, and Providencia spp. are still resistant to tigecycline.

104
Q

What are the Adverse effects of Glycylcyclines and Tetracyclines?

A

GI Irritation and effects on bone and teeth (can lead to an risk of C Difficile) Develops a brown discoloration of teeth NO use for pregnant women – can hurt the babies bone and teeth

105
Q

What are the Aminoglycosides?

A

Streptomycin

Gentamycin

Tobramycin

Amikacin

Neomycin

Paromomycin

106
Q

How do Aminoglycosides inhibit bacteria? (3 ways)

A

Bind to the 30S subunit and inhibit protein synthesis 3 ways: 1) Inhibit imitation of protein by fixing the 50S and 30S ribosomal subunit to the AUG 2) they also inhibit continuation of Translation/ early termination 3) Introduce errors into protein synthesis – nonfunctional proteins

(They are BACTERICIDIAL)

107
Q

How do Aminoglycosides get into bacteria?

A

Through Outer membrane porin channels, relying on the electrical gradient

108
Q

How are Bacteria becoming resistant to Aminoglycosides?

A

1) Enzymatic Inactivation of aminoglycocides
2) Intracellular Transport of Aminoglycosides (due to mutation of porins)
3) Mutations of 30S subunit prevent binding

109
Q

What are the susceptible bacteria to Aminoglycosides?

A

Enterobacter spp., E. coli, Klebsiella pneumoniae, Pseudomonas aeruginosa, Serratia spp., and Acinetobacter baumanii.

(NEVER USE ALONE TO TREAT A GRAM + BACTERIA)

110
Q

What are Aminogylcosides almost always combined with?

A

Beta Lactam Antibiotic

111
Q

What does this Combo of Beta Lactam Antibiotic and Aminoglycosides provide coverage for?

A

Listeria

Viridans

Enterococci

Stapylcocci

112
Q

What are the Adverse effects of Aminoglycosides?

A

Nephrotoxic and Ototoxic (Vestibular Damage, Loss of Balance, Ataxia, Vertigo)

113
Q

What are the Fluoroquinolones?

A

Flourinated analogs of Quinolone nalidixic acid

Moxifloxacin

Ciprofloxacin

Ofloxacin

Gatifloxacin

Gemifloxacin

Levofloxacin

114
Q

What are the groups of Fluoroquinolones and there respective bacteria?

A

Norf, Cipro, Levo, Oflo, Eno, Lome, Peflo – improved activity against Gram +

Gemi, Moxi, Dati, – superior activity of Gram +

Moxi – has action against Anaerobes

115
Q

What were the problems with some Fluoroquinolones?

A

Phototoxicity and QT Prolongation

116
Q

How do Flooroquinolones work?

A

They inhibit transcription and replication of bacterial DNA

INHIBIT Topoisomerase II (DNA Gyrase)

117
Q

How are bacteria becoming resistant to Fluoroquinolones?

A

1) Mutations to quinolone binding site on topoisomerase IV or DNA gyrase
2) Drug Efflux
3) Upreg of proteins that protect the enzymes

118
Q

What are the primary organisms Fluoroquinolones are active against?

A

Fluoroquinolones are potent bactericidal agents against Campylobacter spp., Enterobacter spp., Shigella spp., Salmonella spp., Proteus spp., Klebsiella spp., and E. coli. Fluoroquinolones are also active against intracellular microorganisms including Legionella spp. and Chlamydia spp.

119
Q

Levofloxacin is the __ Isomer of Ofloxacin and has exceptional activity against ___ bacteria (Strep Pneumoniae)

A

L Isomer

Gram + Bacteria

120
Q

Ciprofloxacin is best against __ bacteria (P Aeruginosa)

A

Gram - Bacteria

121
Q

A 3rd group of Fluoroquinoloes are active now: (Moxifloxacin) and is active against what?

A

Effective against some Anaerobes INCREASED activity against Gram +’s – S Pneumoniae and some staph

122
Q

What are the complications of Fluoroquinolones?

A

Abdominal Discomfort, Nausea, Vomiting,

ACHILLES TENDON RUPTURE (rare, but testable)

Moxifloxacin (3rd gen Flouro) – causes QT prolongation, torsades de pointes arrhthymia

123
Q

What is the one Sulfonadmide and Benzylpyrimidine?

A

TMP/SMX (Bactrim) (Sulfamethoxazole-Trimethoprim)

124
Q

How does TMP/SMX work?

A

it inhibits steps in the tetrahydrofolate biosynthetic pathway

125
Q

How does resistance to TMP/SMX work?

A

SMX Resistance

1) Changes to the Bacterial Tetrahydrofolate bio pathway
2) Bacterial overproduction of PABA
3) Reduced Binding
4) Decrease med entry into bacteria (permeability)

TMP Resistance

1) Reduced bacterial permability
2) Upreg of dihydrofolate reductase
3) reduced binding affinity

126
Q

Can Trimethoprim be given as a mono therapy?

A

YES! but rarely – for UTI

127
Q

What bacteria are resistant to Trimethoprim?

A

P Aeruginosa

B Fragilis

Enterococci

128
Q

What bacteria are susceptible to TMP/SMX?

A

A SHIT TON (look in the packet)

129
Q

What are the consequences of TMP/SMX use?

A

Anemia, Leukopenia, Granulocytopenia Nausea, Vomting, Photosensitivty, Fever, Uricaria (hives), Skin Rashes Stevens-Johnson Syndrome

130
Q

What are the main Polymyxins?

A

Colistimethate (Polymyxin B)

Colistin (named Polymyxin E – for topical use)

(was discovered from the Bacillus Polymyxa)

131
Q

How do Polymyxins act against bacteria?

A

disrupt the phospholipid membrane bind to and inactivate endotoxin

ARE BACTERICIDAL

132
Q

What bacteria are resistant to Polymyxins?

A

Extensively drug resistant strains of; Klebsiella, Acinetobacter, Neisseria, Burkholderia, Stenotrophomonas spp Gram + Bacteria (because they don’t have an outer membrane like Gram Neg) Anaerobes

133
Q

What bacteria are Polymyxins active against?

A

Enterobacteriaceae

Pseudomonas spp

Acinetobacter spp

Proteus spp

Serratia spp

(Good for superficial cuts and scraps)

134
Q

What are the problems with taking Polymyxins?

A

Nephrotoxicity

Slurred Speech

Vertigo

Paresthesias

Apnea

Muscle Weakness

MOD Exam III - Antibiotics (1 decks)

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