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Immuno mikro eng > Pharmacology of Antimicrobials: Everything Else > Flashcards

Pharmacology of Antimicrobials: Everything Else Flashcards

1
Q

What is the mechanism of action of aminoglycosides and how do you remember this?

A

Bind the 30S subunit of the ribosome to decrease protein synthesis

AT = small, AT base pairing, both aminoglycosides and tetracyclines bind the small 30S subunit

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2
Q

Are aminoglycosides cidal or static, and why don’t they have activity against anaerobes?

A

Cidal - exception to rule of protein synthesis inhibitors

No activity against anaerobes because they require active transport into the cell

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3
Q

What are aminoglycosides mainly used for?

A

They have a synergistic effect, combine with a Beta-lactam because cell wall interruptors help more enter the cell

Expands Beta-lactam spectrum to enterococcus (Facultatitive anaerobes), typically only used in serious infections

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4
Q

What is gentamicin’s route and when is it used?

A

Typically IV - used synergistically for serious staph / enterococcal infections (i.e. endocarditis)

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5
Q

What is tobramycin’s route and when is it used?

A

IV - empiric coverage of nosocomial infections (used with Zosyn or mirapenem or cefepime)

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6
Q

What is amikacin’s route and when is it used?

A

Also empiric coverage of nosocomial infections, but has some role in mycobacterial infections

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7
Q

What is Neomycin’s role and why?

A

Neomycin is taken PO to decontaminate GI tract prior to surgery since it is not absorbed PO

Topically, it is neosporin

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8
Q

When is streptomycin used?

A

IV, when gentamycin resistant, and like amikacin for mycobacterial infections

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9
Q

Why are aminoglycosides good for UTI’s?

A

Hydrophilic (limited tissue penetration), but good for high urine concentrations and kidney excretion

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10
Q

What are two resistance mechanisms for aminoglycosides?

A
  1. Enzymatic modification - add a side chain which prevents 30S ribosomal binding = drug specific
  2. Target-site modification - modification of 30S ribosome, loss of entire class
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11
Q

What is the most common side effect of aminoglycosides and how can this be reduced?

A

Nephrotoxicity -> reduce trough levels at end of dosing intervals, letting tubules regrow

Less commonly: irreversible deafness due to vestibular / ototoxicity

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12
Q

What is the mechanism of action of fluoroquinolones, and is it cidal or static?

A

Inhibit bacterial DNA replication via inhibition of topoisomerases

It is bactericidal

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13
Q

What are the fluoroquinolones of clinical significance?

A

Ciprofloxacin
Levofloxacin
Moxifloxacin

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14
Q

What are levofloxacin and moxifloxacin also called and why?

A

Respiratory fluoroquinones -> good against all streptococcus, and all CAP organisms

Should not be relied on vs Staph / Enterococcus due to easy mutation

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15
Q

What is Ciprofloxacin good for?

A

Good against gram negative, with anti-pseudomonal activity (resistance in place in respiratory bugs, unfortunately)

So is levofloxacin, so we don’t carry it for its overuse potential

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16
Q

What is B. fragilis and what fluoroquinone is good against it?

A

An anaerobe commonly targeted in therapies

Only moxifloxacin

Unfortunately, it lacks anti-pseudomonal activity

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17
Q

What is the route of delivery for fluoroquinones?

A

Orally -> excellent bioavailability

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18
Q

How are the fluoroquinolones cleared and why is this relevant?

A

Cleared via kidney, however moxifloxacin is not so it can’t be used versus UTIs

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19
Q

What are the common fluoroquinolone side effects?

A

CNS toxicity - headaches, seizures, neuropathies
Tendon ruptures due to cartilage damage
Dysglycemia
Cardiac arrythmias / prolonged QT, especially moxifloxacin

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20
Q

What is a critical drug interaction with FQ?

A

Reduced divalent cation absorption due to chelation

-> separate 2-4 hours

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21
Q

Why are FQ so dangerous for developing resistance?

A

Cause development of efflux pumps which can also efflux Abx of unrelated structures

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22
Q

What class is vancomycin and what is its mechanism of action? Cidal or static?

A

Glycopeptide, works by binding D-ala,D-ala portion of peptidoglycan, preventing further cross-linking

Very slowly cidal (weak killing)

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23
Q

What organisms does vancomycin cover?

A

Gram positive only, used for empirical MRSA coverage (inferior for MSSA), in patients with Beta-lactam allergy who need gram + coverage

Very broad spectrum

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24
Q

When would you not need to empirically treat for MRSA with vancomycin?

A

Whenever the condition of the patient is not that serious and you can wait for a culture

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25
Q

What is Red-Man’s Syndrome?

A

Histamine-response to vancomycin often caused by too rapid infusion

Prevented by diphenhydramine or not infusing greater than 1g/hr

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26
Q

What is the side effect of concern for vancomycin?

A

Nephrotoxicity - 10-15%, especially in obese patients

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27
Q

What is the second generation glycopeptide and why isn’t it used?

A

It is a LIPOglycopeptide called telavancin, also disrupts membrane barrier function.

Not used due to even higher nephrotoxicity + interference with coagulation tests

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28
Q

What are dalbavancin and oritavancin?

A

Long-acting glycopeptides which are being studied for skin infections, huge potential for single dose therapies being entire drug course

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29
Q

What is daptomycin’s mechanism of action and killing activity? How is it given?

A

IV only - highly bactericidal to gram + organisms only

It uses its lipid tail to build a pore in cell membrane (like MAC) and osmotically lyse the cell

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30
Q

What is the major clinical use of daptomycin?

A

MRSA and VRE bloodstream infections (only with high levels of resistance, intermediate = VISA = cell wall thickening giving cross-resistance), endocarditis, soft tissue infections

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31
Q

What are daptomycin’s issues and when is it absolutely contraindicated?

A

Causes CPK elevations and rhabdomyolysis (muscle breakdown)

Irreversibly binds pulmonary surfactant, avoid in pneumonia

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32
Q

In what class is oxazolidinone and what is its mechanism of killing / activity?

A

Linezolid

Inhibits protein synthesis via 50S ribosome, bacteriostatic effect

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33
Q

What is the clinical application of Linezolids?

A

VRE infections - but keep in mind it’s only static

MRSA - pneumonia (when vanco-resistant, dapto can’t be used)

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34
Q

Why are linezolid’s so perfect?

A

IV / PO dose is the same, and it’s not renally eliminated so dosage is not needed to be adjusted

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35
Q

What is the major side effect of concern for linezolid?

A

Thrombocytopenia, especially in long courses

36
Q

What is the major drug interaction of linezolid?

A

It is a weak MAOI, so can cause serotonin syndrome with SSRIs (fever, agitation, mental status change)

37
Q

What are VRE and what is the most common species for it? How is it typically treated?

A

Vancomycin-resistant enterococcus

Common in Enterococcus faecium

Treated via Linezolid / Daptomycin usually

38
Q

What is the VRE mechanism?

A

D-ala, D-ala becomes D-ala, D-lac (or D-ser), which Vanco cannot bind

39
Q

Why is Oritavancin still useful against VRE?

A

Can bind D-lac as well

40
Q

Why is VRSA very rare? What is good against it?

A

very expensive for resistance mechanism

Daptomycin is good against it

41
Q

What was the first drug for treatment of VRE? Why has it fallen out of favor?

A

A streptogramin called Synercid (quinupristin / dalfopristin), binds 50S ribosome

Fallen out of favor due to high rates of infusion reactions

42
Q

What are the macrolides / mechanism of action / killing?

A
  1. Azithromycin (IV/PO)
  2. Clarithromycin (PO)
  3. Erythromycin (IV/PO)

Bind 50S ribosome
Bacteriostatic

43
Q

What are the macrolides mostly active against?

A

Respiratory pathogens, including pneumococcus, Hemophilus, mycobacterium

Also: Chlymadia / gonorrhea
Mycobacterium avium complex seen in HIV

44
Q

What is Clarithromycin mainly used for?

A

Standard therapy for H. pylori

45
Q

What is Azithromycin used for? Why is it chosen most often?

A

Chlymadia, gonorrhea, non-TB mycobacteria, and 1st line for CAP

It has a long half life, allowing for shorter drug course

46
Q

Why is erythromycin not really used anymore?

A

Binds to motilin receptor in GI tract and causes diarrhea

47
Q

What are the side effects of concern for the macrolides?

A

Nausea, vomiting, and diarrhea are very common

Also QT prolongation

48
Q

Why is azithromycin chosen most often?

A

Has a long half life for short regimens, IV dose = PO dose, and it has the fewest CYP3A4 interactions

49
Q

What is the mechanism of action and killing of tetracyclines?

A

Works on 30S ribosome, bacteriostatic

50
Q

What are the clinical tetracyclines and their route?

A

Tetracycline - PO
Doxycycline / Minocycline (IV/PO)
Demeclocycline - PO

51
Q

What is Demeclocycline used for?

A

Treatment of SIADH (inappropriate ADH release)

52
Q

What are the side effects of tetracyclines?

A
  1. Bind to growing teeth and bones (do not use in patients under 8 years)
  2. Photosensitization
53
Q

What are the drug interactions with tetracyclines?

A

Chelate with divalent and trivalent cations (like FQs)

54
Q

What are doxycycline / minocycline typically used for?

A

Respiratory tract infections, including CAP
Skin infections, especially when CA-MRSA is a concern

Good against animal bites / lyme disease

55
Q

What is minocycline emerging as good for?

A

Carbapenem-resistant A. baumannii

56
Q

What is Tigecycline?

A

A glycylcycline, a derivative of minocycline binding 30S ribosome which can overcome tetracycline resistance mechanisms

57
Q

What are the two big problems with tigecycline?

A
  1. Highly lipophilic - poor for treating blood, lung, and urine infections
  2. Causes nausea/vomiting in 20% of patients
58
Q

What is the spectrum of tigecycline activity? When is it used clinically?

A

Very broad in both gram positive and negative, just misses PP = pseudomonas and proteus

Used as last line for resistant gram-negative like Acetinobacter and Klebsiella

Used often in POLYMICROBIAL WOUNDS including MRSA or VRE

59
Q

What is the major lincosamide and its killing type?

A

Clindamycin

50S subunit -> bacteriostatic

60
Q

What does clindamycin ideally cover, and what is one fun fact about it?

A

Staph, strept, and oral anaerobes (unfortunately minus B. fragilis), (no gram negative), though effectiveness is waning

Has toxin suppression activities against necrotizing gram + infections

61
Q

What is the major side effect of clindamycin?

A

C. difficile diarrhea -> was once the number one antibiotic associated with it

62
Q

What are the major intended uses of Clindamycin?

A 
Skin infections
Aspiration pneumonia (especially because anaerobes are thought to be players, but no gram negative coverage)
63
Q

What is the significance of the “erm” gene?

A

Encodes “MLS” resistance to Macrolides-Lincosamides-Streptogramin, which all act on 50S ribosome, and give S. aureus a huge resistance mechanism

64
Q

What should be done if something is found to be erythromycin resistant but clindamycin susceptible?

A

Special “D test”, since resistance may be latent and inducible

65
Q

How do sulfonamides work? Most common one?

A

Structural analogs of PABA, blocking DHF synthesis from PABA competitively

Sulfamethoxazole, bacteriostatic

66
Q

What is Sulfamethoxazole often combined with and how are they synergistic?

A

Combined with trimethoprim, another static inhibitor working on DHF reductase for DNA synthesis

As TMP / SMX, it is called bactrim and BACTERICIDAL

67
Q

What is the major clinical role for TMP/SMX?

A

Outpatient UTIs, good against MRSA but poor for Strept (not good for skin infections)

68
Q

What two nasty infections can TMP/SMX treat?

A

Pneumocystic (jirovecii) pneumonia, and Stenotrophomonas maltophilia pneumonia

69
Q

What are the side effects of “sulfa drugs” = TMP/SMX?

A

Hypersensitivity, often severe skin reactions

Stops kidney creatinine excretion, causing creatinine to rise

70
Q

What can Trimethoprim cause?

A

Hyperkalemia -> blocks K+ excretion, so beware with K+ sparing diuretics

Also anemia, leukopenia, and granulocytopenia

Increased bleeding when given with warfarin

71
Q

What is the main nitro-imidazole given? How does it relate to clindamycin?

A

Metronidazole - good for GI anaerobes vs clindamycin which was good for oral anaerobes

72
Q

What are three main uses of metronidazole?

A
  1. Empiric anaerobic coverage for intra-abdominal infections
  2. Drug of choice for mild-moderate C. difficile
  3. Trichomonas vaginalis coverage
73
Q

What is the major side effect of metronidazole?

A

Peripheral neuropathy if given cumulatively

74
Q

What are the drug interactions with metronidazole?

A
  1. Warfarin reaction (increased bleeding)

2. Alcohol - Disulfiram reaction with any consumption (like MTT-containing cephalosporins)

75
Q

What is the mechanism of action of Rifampin?

A

Binds the DNA-dependent RNA polymerase, blocking bacterial mRNA synthesis

76
Q

What is Rifampin’s spectrum of activity?

A

Good against all gram +, including MRSA, but not used as a monotherapy

Ineffective against gram negative unless in combination

Excellent against TB

77
Q

In what clinical scenarios is Rifampin actually used?

A

Part of standard TB regimen, against staph infections complicated by hardware / biofilms, and against MDR gram negative

78
Q

Give two reasons why Rifampin is not typically used

A
  1. Hepatotoxicity
  2. Induces multiple Cytochrome P450 enzymes, including CYP3A4. Contraindicated in many HIV meds because it causes subtherapeutic levels of the drugs (quicker metabolism)
79
Q

What is one side effect you must warn patients of with Rifampin?

A

They will have discolored fluids

80
Q

How do polymyxins work? Static or cidal?

A

Cationic detergents which interact with LPS on gram negative organisms, displacing divalent cations and disrupting outer membrane

Has anti-endotoxin effect and is bactericidal

81
Q

What is the major polymyxin used and why did it stop being used?

A

Polymyxin B, can be IV, PO, or topical

Stopped being used due to nephrotoxicity (like vanco and aminoglycosides) and neurotoxicity

82
Q

Why is polymyxin used clinically?

A

Last line treatment against multi-drug resistant gram negative:

P. aeruginosa, A. baumanii, K. pneumoniae, E. coli

83
Q

Why is chloramphenicol not used anymore?

A

Caused bone marrow suppression, aplastic anemia, and gray-baby syndrome (toxic phase 2 metabolite)

84
Q

What is nitrofurantoin used for, and its main contraindication?

A

Urinary tract organisms (gram negative, narrow spectrum)

Contraindicated if GFR < 60 mL/min (compromised kidney function)

85
Q

What is the mechanism of action of dapsone and when is it used?

A

antagonist of PABA

Used in prevention and treatment of pneumocystic pneumonia when patient has sulfa allergy (can’t used TMP/SMX)

86
Q

What is the major side effect of dapsone?

A

Hemolysis which is much worse in G6P dehydrogenase deficiency

Immuno mikro eng (56 decks)

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