Infectious Dz - Antibiotic Review Flashcards

(103 cards)

1
Q

What do bacteriostatic antibiotics do?

A

They stop bacterial growth by interfering with protein synthesis and metabolism

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2
Q

What do bactericidal antibiotics do?

A

The kill bacteria by interfering with cell wall or nucleic acid synthesis

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3
Q

What antibiotics are bacteriostatic?

A

Chloramphenicol, sulfanomides, trimethoprim, clindamycin, doxycycline, and macrolides

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4
Q

What antibiotics are bactericidal?

A

Beta-lactams, fluoroquinolones, aminoglycosides, Timethoprim sulfas (which is the combo of sulfanomides and trimethoprim), vancomycin, and metronidazole

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5
Q

When will the classification of an antibiotic (static or cidal) influence your choice of antibiotic?

A

If there are life-threatening infections or an immunocompromised individual

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6
Q

What is the minimum inhibitory concentration (MIC)?

A

The lowest concentration of an antimicrobial that will inhibit bacterial growth

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7
Q

What factors does the in vitro value not take into account?

A

In vivo factors - Antibody in the serum, urine, and bile, pH of the infected environment, and presence of biofilms

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8
Q

What is efficacy of an antibiotic related to?

A

the amount of time that the antibiotic concentration is above the MIC

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9
Q

What maximizes efficacy of antibiotics?

A

Multiple daily doses, continuous administration, OR giving a single daily (high) dose

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10
Q

What antibiotics are time-dependent?

A

Penicillins, cephalosporins, carbapenems, macrolides, lincosamides, and tetracyclines

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11
Q

What antibiotics are concentration dependent?

A

Fluoroquinolones, aminoglycosides, and metronidazole

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12
Q

What four antibiotics/groups are part of the beta lactam structural group?

A

Penicillins, cephalosporins, carbapenems, and monobactams

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13
Q

Are the beta lactams cidal or static? Time or concentration dependent?

A

Cidal and time-dependent

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14
Q

How do beta lactams work?

A

They block cell wall synthesis by inhibiting penicillin-binding proteins

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15
Q

How are beta lactams metabolized?

A

They are renally excreted - high concentrations in the urine

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16
Q

What forms of penicillin do we use in small animals?

A

Amoxicillin/ampicillin and Ticarcillin

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17
Q

What is the spectrum of activity of penicillins?

A

Excellent activity against Gram + and anaerobes
Some gram - efficacy
Not effective against Pseudomonas

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18
Q

What enzyme do gram - bacteria produce that inactivates beta-lactam antibiotics?

A

Beta lactamase

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19
Q

What can extend the efficacy of penicillins against beta lactamase inhibitors?

A

Clavulanic acid (Clavamox) and Sulbactam (Unasyn)

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20
Q

What generation of cephalosporins has the most activity against gram negative organisms?

A

4th generation - activity increases with the generation

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21
Q

What is the spectrum of cephalosporins?

A

Effective against Gram positives

Resistant to all Gram + beta-lactamases

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22
Q

What carbapenems are used in small animal medicine?

A

Imipenem and Meropenem

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23
Q

What ‘effect’ do carbapenems have that other beta-lactams don’t have?

A

a post-antibiotic effect

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24
Q

What are Carbapenems effective against?

A

Gram negative and positive bacteria - there is little resistance as of now because these drugs are reserved for serious infections (the big guns)

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25
How are Carbapenems formulated?
In IV and SQ routes because there is poor oral absorption
26
Uses of Carbapenems should be limited to what?
Serious multi-drug resistant gram - infections and in immunocompromised individuals
27
What glycopeptide do we use in small animal medicine?
Vancomycin
28
Is Vancomycin static or cidal? Time or concentration dependent?
Cidal and time-dependent
29
How do glycopeptides work?
They inhibit cell wall synthesis by binding amino acids used in its synthesis
30
How are glycopeptides formulated?
IV due to poor oral absorption
31
When is it recommended to use glycopeptides?
Only for multi-drug resistant gram + infections - Clostridium difficile and Methicillin-resistant Staph infections
32
What are the adverse effects of glycopeptides?
Red man syndrome (humans) and nephrotoxicity
33
Are fluoroquinolones cidal or static? Time or concentration dependent?
Cidal and concentration-dependent
34
How do fluoroquinolones work?
They cause disruption of DNA synthesis by inhibition of DNA gyrase and topoisomerase IV
35
What fluoroquinolones do we use in small animal medicine?
Marbofloxacin, enrofloxacin, ciprofloxacin, and pradofloxacin
36
What is the spectrum for fluoroquinolones?
Gram - bacteria, but also effective against + at higher doses Poor efficacy against anaerobes Attains high intracellular concentration which is good for Mycoplasma
37
What infections are fluoroquinolones good for and why?
They are highly lipophilic which provides for excellent penetration for prostatic and respiratory infections
38
What are the adverse effects of enrofloxacin in cats?
Acute retinal degeneration
39
What is a safer fluoroquinolone in cats?
pradofloxacin
40
What adverse effects do fluoroquinolones cause in young animals (4-28 weeks)?
Cartilage/joint toxicity
41
What does pradofloxacin cause when given in high doses in dogs?
Myelosuppression
42
Is metronidazole static or cidal? Time or concentration dependent?
Cidal and concentration dependent
43
How does metronidazole work?
It is a prodrug that is activated in the bacterial cytoplasm to a free radical that causes DNA damage
44
What is the spectrum of metronidazole?
It is especially effective against anaerobes (both gram + and - ) and protozoans (Giardia)
45
What are the adverse effects of metronidazole?
Neurotoxicity with higher doses - there are generally vestibular signs
46
True or False: Sulfonamides are always combined with trimethoprim
True
47
What is the MOA of trimethoprim-sulfonamide (TMS)?
Synergistic inhibition of folate metabolism, resulting in inhibition of purine synthesis
48
What enzyme does trimethoprim produce?
dihydrofolate reductase
49
What enzyme does sulfonamide produce?
pteridin synthase
50
What are sulfonamides effective against?
Gram + and - bacteria - especially Nocardia Protozoal organisms Variable efficacy against anaerobes
51
Where do sulfonamides have excellent penetration?
in prostatic tissue
52
Where are sulfonamides in high concentration?
urine
53
What are the adverse effects of sulfonamides?
KCS, immune-mediate thrombocytopenia, hemolytic anemia/aplastic anemia, polyarthritis, hepatotoxicity, and bone marrow suppression
54
How should you monitor for adverse effects of sulfonamides?
Shirmer tear test, liver panels, and CBC
55
What aminoglycosides do we use in small animal medicine?
Amikacin, gentamicin, tobramycin, and neomycin
56
What is the MOA of aminoglycosides?
Interfere with outer membrane LPS structure and inhibit protein synthesis by binding to the 30S ribosomal subunit
57
Are aminoglycosides static or cidal? Time or concentration dependent?
cidal and concentration dependent
58
What organs do the aminoglycosides have poor penetration into?
The prostate, brain/CSF, and the eye
59
What is the spectrum of aminoglycosides?
Excellent gram - activity, good gram + activity | Anaerobes have intrinsic resistence
60
How are aminoglycosides formulated?
SC, IM, IV, or topical administration because there is poor oral administration
61
Where are aminoglycosides excreted?
in the urine
62
What are the adverse effects of aminoglycosides?
Nephrotoxicity and ototoxicity
63
What chloramphenicols are used in small animal medicine?
Chloramphenicol, florfenicol and thiamphenicol
64
What is the MOA of chloramphenicols?
Inhibits protein synthesis by binding to the 50S ribosomal subunit
65
Are chloramphenicols static or cidal? time or concentration dependent?
Static and time dependent
66
What is the spectrum of chloramphenicols?
Broad spectrum - gram +/- and anaerobes
67
What organs do chloramphenicols have excellent penetration?
Brain, eye, and prostate due to excellent lipid sollubility
68
What are the adverse effects of chloramphenicols?
Irreversible aplastic anemia in humans | Reversible bone marrow suppression
69
What species are chloramphenicols poorly tolerated in?
cats - they get GI signs and BM suppression
70
What tetracyclines do we use in small animal medicine?
tetracycline, doxycycline, and minocycline
71
Are tetracyclines static or cidal? Time or concentration dependent?
Static and time dependent
72
What is the MOA of tetracyclines?
Inhibits protein synthesis by binding 30S ribosomal subunit
73
What is the spectrum of tetracyclines?
Gram + and - intracellular bacteria (rickettsiae) and spirochetes
74
What are the adverse effects of tetracyclines?
vomiting, esophagitis and esophageal strictures in cats, hepatopathy, and possible dental discoloration with use of doxy
75
What lincosamides do we use in small animal medicine?
Clindamycin and lincomycin
76
Are lincosamides static or cidal? Time or concentration dependent?
Static and time dependent
77
What is the MOA of lincosamides?
inhibits protein synthesis by binding to 50S ribosomal subunit
78
What is the spectrum of lincosamides?
Gram postitives, anaerobes, and protozoans
79
What are the adverse effects of lincosamides?
Esophagitis in cats
80
What macrolides do we use in small animal medicine?
Erythromycin, tylosin, clarithromycin, and azithromycin
81
Are macrolides static or cidal? Time or concentration dependent?
Static and time dependent
82
What is the spectrum of macrolides?
Gram +, some gram -, and mycobacterium (clarithromycin)
83
What macrolide is good for antibiotic resistant diarrhea?
tylosin
84
Are fungi eukaryotes or prokaryotes?
eukaryotes
85
What antifungals do we use?
Azoles, amphotericin B, 5-flucytosine, and terbinafine
86
What imidazoles do we use in small animal medicine?
Ketoconazole, clotrimazole, and enilconazole
87
What triazoles do we use in small animal medicine?
Itraconazole, fluconazole, voriconazole, and posaconazole
88
Do imidazoles or triazoles have more side effects?
imidazoles
89
What is the MOA of azoles?
They are fungistatic - interfere with ergosterol synthesis through inhibition of 14 alpha-demethylase
90
What are the adverse effects of azoles?
``` Inhibition of mammalian p450 Suppression of adrenal function (ketoconazole) Teratogenic Hepatotoxicity Ulcerative skin lesions (itraconazole) ```
91
What is the MOA of Amphotericin B?
Causes pores in the cell membrane by binding to sterols | Macrophage activation
92
Is amphotericin B static or cidal?
Static but cidal at high doses
93
What are the adverse effects of amphotericin B?
nephrotoxicity
94
What is the MOA of 5-Flucytosine?
It is a fluorinated pyrimidine that interferes with DNA replication when converted to fluorouracil
95
What is 5-Flucytosine effective against?
Only against Cryptococcus and Candida
96
Is 5-Flucytosine static or cidal?
static
97
Why is 5-Flucytosine never used alone?
Because resistance develops quickly when used as a single agent
98
What are the adverse effects of 5-Flucytosine?
Cutaneous drug eruptions (dogs) and myelosuppression
99
How does Terbinafine work?
It inhibits squalene epoxidase, causing intracellular accumulation of squalene
100
Is terbinafine static or cidal?
cidal
101
What is terbinafine especially effective against?
dermatophytes
102
What are the adverse effects of terbinafine?
Most are unknown, but it is known to cause facial pruritus in cats
103
You are treating a 15 year old spayed female cat with a suspected UTI. Which antibiotic would be the best choice for treatment? a. Enrofloxacin b. Gentamicin c. Amoxicillin d. Chloramphenicol
c. Amoxicillin Not enrofloxacin because it causes acute retinal degeneration in cats Not Gentamicin because.... not entirely sure, but it does cause nephrotoxicity Not Chloramphenicol because it is poorly tolerated in cats