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Pharmacology > Anti-Infective Agents > Flashcards

Anti-Infective Agents Flashcards

1
Q

Parasitic worm infections are also called what?

A

helminth infections

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2
Q

Parasitic Infections include what specifically?

A
  • roundworms (flukes)
  • tapeworms
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3
Q

Where are parasitic infections common?

A
  • common in tropical, poor rural areas
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4
Q

How are specific diagnostics performed for parasitic infections?

A
  • often involve evaluating stool/feces for eggs
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5
Q

How do antihelmintics act in the body?

A
  • act locally within the gut or systemically for those that infect other locations
  • they expel parasitic worms and other internal parasites from the body by either stunning or killing them and without causing significant damage to the host
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6
Q

Antihelmintic Agents

A
  1. Albendazole
  2. Ivermectin
  3. Nitazoxanide
  4. Praziquantel
  5. Pyrantel
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7
Q

Side effects of Pyrantel

A
  • nausea
  • vomiting
  • diarrhea
  • abdominal pain
  • heachache
  • rash
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8
Q

Antibacterial Agents

A
  • development of new agents to keep up with patterns of resistance
  • resistance develops as a “survival” mechanism for bacteria, disabling the antibiotic
  • therapeutic drug monitoring can prevent toxicity and can ensure appropriate drug dose
  • watch for avoidable food and drug interactions that may contribute to suboptimal therapy
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9
Q

How do penicillins act in the body?

A
  • can easily enter bacterial cell in case of gram-positive species
  • gram-positive bacteria do not have an outer cell membrane and are simply enclosed in a thick cell wall
  • PCN molecules are small enough to pass through the spaces of glycoproteins in the cell wall
  • gram-positive bacteria are very susceptible to PCN
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10
Q

Gram-positive bacterias

A
  1. Staphylococcus
  2. Streptococcus
  3. Enterococcus
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11
Q

Characteristics of PCN

A
  • 10% cross-sensitivity with cephalosporins
  • low plasma protein binding capacity
  • short half-life (requires multiple x/day dosing)
  • excreted by the kidneys
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12
Q

Side Effects of PCN

A
  • diarrhea
  • nausea
  • rash
  • superinfection (candidiasis)
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13
Q

PCN Resistance

A
  • E. coli produced specific enzymes that can break down pcn molecule “Penicillinase” aka B-lactamase
  • B-lactamases is the most important mechanism of pcn resistance
  • B-lactamase inhibitors prevent the bacterial degradation of beta lactam antibiotics and extend the rage of bacteria drugs are effective against
  • B-lactamase inhibitors have little antibiotic activity on their own
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14
Q

Characteristics of Cephalosporins

A
  • beta-lactam antibiotic
  • most commonly prescribed drugs
  • broad-spectrum antibiotic coverage
  • less susceptible to beta-lactamase
  • disrupt the synthesis of the peptidoglycan layer forming the bacterial cell wall
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15
Q

Side Effects of Cephalosporins

A
  • N/V/D
  • rash
  • pain at the injection site
  • superinfection (10% cross-sensitivity)
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16
Q

1st Generation Cephalosporins

A
  • oldest cephalosporins
  • active against gram-positive cocci
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17
Q

1st generation cephalosporins are not useful against what?

A
  • enterococci
  • listeria
  • MRSA
  • gram-negative cocci (gonococcus, meningococcus)
  • H. influenza
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18
Q

1st generation cephalosporins are effective against what?

A
  • E. coli
  • Proteus mirabilis
  • Klebsiella pneumonia
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19
Q

Examples of 1st generation cephalosporins

A
  • Cefadroxil
  • Cefazolin
  • Cephelaxin
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20
Q

2nd Generation Cephalosporins are less active against what?

A
  • less active against staphylococci and enhanced activity against H-influenza
  • weak gram-positive coverage
  • strong gram-negative coverage
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21
Q

2nd Generation Cephalosporins are active against what?

A
  • cephamycins (subgroup) are active against Bacteroides
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22
Q

Examples of 2nd generation cephalosporins

A
  • Cefaclor
  • Cefprozil
  • Cefuroxime
  • Cefotetan
  • Cefoxtin
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23
Q

3rd Generation Cephalosporins

A
  • marked by stability to the common B-lactamases of gram-negative bacilli, and these compounds are highly active against Enterobacteriaceae, Neisseria, and H. influenza
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24
Q

Examples of Enterobacteriaceae that 3rd generation cephalosporins are active against

A
  • E. coli
  • Proteus mirabilis
  • indole-positive Proteus
  • Klebsiella
  • Enterobacter
  • Serratia
  • Citrobacter
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25
Q

4th Generation Cephalosporins

A
  • has good penetration through outer membrane of gram-negative bacteria
  • similar activity to cefotaxime and ceftriaxone
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26
Q

Example of 4th generation cephalosporins

A
  • Cefepime
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27
Q

4th generation cephalosporins are active against what?

A

Pseudomonas aeruginosa

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28
Q

Side effects of 4th generation cephalosporins

A

Superinfection
- enterocci
- candida

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29
Q

Cholramphenicol

A
  • useful against typhoid and conjunctivitis
  • no longer recommended by WHO as first-line to treat meningitis
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30
Q

Side effects of cholramphenicol

A
  • bone marrow suppression
  • aplastic anemia
  • leukemia
  • N/V
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31
Q

Characteristics of Macrolides

A
  • natural product consisting of a large macrocyclic ring
  • are bacteriostatic in that they suppress or inhibit bacterial growth rather than killing bacteria completely
  • are protein synthesis inhibitors
  • wider antibiotic spectrum than penicillins
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32
Q

Macrolides are useful treating what?

A
  • used to treat infections by gram-positive bacteria (PCN allergic patients), community acquired respiratory tract infections, and mycobacterial infections
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33
Q

Examples of Macrolides

A
  1. Azithromycin
  2. Clarithromycin
  3. Erythromycin
  4. Fidaxomicin
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34
Q

Side Effects of Macrolides

A
  • clarithromycin and erythromycin are potent inhibitors of CYP3A4 and cause QT prolongation which can lead to Torsades de Pointes
  • exhibit enterohepatic recycling
  • can also cause cholestasis and Infantile pyloric stenosis
  • given with colchicine may lead to colchicine toxicity
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35
Q

What is enterohepatic recycling?

A
  • drugs absorbed by the gut sent to the liver, excreted into the duodenum in bile from the liver, leading to build up
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36
Q

Characteristics of Aminoglycosides

A
  • display concentration-dependent bactericidal activity against “most gram-negative aerobic and facultative anaerobic bacilli”
  • act by binding to aminoacyl site of ribosomal RNA
  • require only short contact time, and are most effective against susceptible bacterial populations that are rapidly multiplying
  • less toxic and do not require serum drug concentration monitoring
  • 99% of the administered dose eliminated unchanged in the urine
37
Q

When to prescribe aminoglycosides as monotherapy

A
  • important as a second agent in treating serious infections
  • sepsis
  • osteomyelitis
  • severe complicated UTI
  • nosocomial respiratory infections
  • abdominal infections
38
Q

Peak serum concentration of aminoglycosides

A

30-90 minutes after IV/IM administration

39
Q

Side Effects of Aminoglycosides

A
  • nephrotoxicity varies widely but can be 10-20% and reversible in most cases
  • ototoxicity may result in either vestibular or cochlear damage
  • avoid in myasthenia gravis due to rare but serious neuromuscular blockade
40
Q

Examples of Aminoglycosides

A
  1. Amikacin
  2. Gentamicin
  3. Neomycin
  4. Streptomycin
  5. Tobramycin
  6. Paromomycin
41
Q

Characteristics of Fluoroquinolones

A
  • are highly effective antibiotics with many advantageous pharmacokinetic properties including high oral bioavailability, large volume of distribution, and broad-spectrum antimicrobial activity
  • are bactericidal that directly inhibit bacterial DNA synthesis
  • food does not substantially reduce absorption
  • renally eliminated
42
Q

What are Fluoroquinolones useful against?

A
  • gram positive
  • gram negative
  • anaerobes
  • atypicals
  • mycobacteria
  • GU infections
  • hospital-acquired CAUTI
  • pneumonia
  • pyelonephritis
  • prostatitis
43
Q

Adverse Effects of Fluoroquinolones

A
  • C. difficile
  • tendinopathy
  • neuropathy
44
Q

Black Box Warning for Fluoroquinolones

A
  • tendon rupture (higher among people > 60 years old)
  • aortic dissection
  • C. dificille colitis
  • worsening of myasthenia gravis symptoms
45
Q

Fluoroquinolone Toxicity

A
  • blockade of GABa receptor complex in the CNS
46
Q

Examples of Fluoroquinolones

A
  1. Ciprofloxacin
  2. Finafloxacin
  3. Gemifloxacin
  4. Levofloxacin
  5. Maxifloxacin
  6. Ofloxacin
47
Q

Fluoroquinolones Contraindications

A
  • epilepsy
  • Marfan’s syndrome
  • Ehlers-Danlos Syndrome
  • QT prolongation
  • pre-existing CNS lesions or inflammation
  • prior CVA
  • avoid in pregnancy
48
Q

Characteristics of Sulfonamides

A
  • act as competitive inhibitors dihydropteroate synthase (DHPS) involved in folate synthesis
  • are bacteriostatic inhibiting growth and multiplication of bacteria but not killing them
  • allergies to sulfonamides are common (3%)
49
Q

Sulfonamides that are devoid of antibacterial activity

A
  • the anticonvulsant sultiame
  • sulfonylureas
  • thiazide diuretics
50
Q

Examples of Sulfonamides

A
  1. Sulfadiazine
  2. Sulfamethoxazole/trimethoprim
  3. Sulfasalazine
51
Q

Sulfonamides are effective against what kind of microorganisms?

A
  • gram-positive bacteria
  • gram-negative bacteria
  • some protozoa
  • toxoplasma species
  • chlamydia
  • nocardia
52
Q

Sulfonamides are effective against what diseases?

A
  • staph aureus
  • strep pneumonia
  • strep pyogenes
  • proteus mirabilis
  • E. coli
  • Salmonella
  • klebsiella
  • pseudomonas
  • N. gonorrheae
  • listeria
53
Q

Side Effects of Sulfonamides

A
  • Stevens-Johnsons syndrome
  • toxic epidermal necrolysis
  • the DRESS syndrome
54
Q

Miscellaneous Urinary Anti-Infectives

A
  1. Fosfomycin
  2. Methenamine
  3. Nitrofurantoin
  4. Trimethoprim (but most often in conjunction with sulfamethoxazole and has a synergistic effect causing it to be bacteriocidal
55
Q

Antifungal Agents

A
  • fungal infections becoming more common with increasing states of immunosuppression (chemotherapy, HIV, etc.)
  • opportunistic fungal infections have also demonstrated resistance and mutation
  • multiple agents with different mechanisms of action are available for use
  • many agent are susceptible to drug interactions involving liver metabolism and competition with other drugs using same “hepatic” pathway
56
Q

Allylamines

A
  • antifungal that are used to kill fungi to treat athlete’s foot, jock itch, ringworm, and nail fungus (dermaphytes)
  • topical activity working to inhibit fungal growth
57
Q

Dermaphytes

A
  • microsporum
  • trichophyton
  • molds (aspergillus)
58
Q

Examples of Allylamines

A
  1. Terbinafine
59
Q

Side Effects of Allylamines

A
  • rash
  • diarrhea
  • vomiting
  • increased liver enzymes
  • hepatic failure
  • headache
  • cough
  • ototoxicity
60
Q

Azoles

A
  • antifungal
  • blocks CYP450 dependent enzymes interrupting the cellular membrane of fungi
61
Q

What do azoles treat?

A
  • candidiasis
  • aspergillosis
  • cryptococcosis
  • histoplasmosis
  • blastomycosis
  • coccidioidmycosis
62
Q

Examples of Azoles

A
  1. Fluconazole
  2. Itraconazole
  3. Voriconazole
  4. Posaconazole
63
Q

Side Effects of Azoles

A
  • GI (N/V/D, abd pain)
  • hepatotoxicity
64
Q

Echinocandins

A
  • antifungal
  • inhibits enzyme activity in the fungal cell wall
  • synergistic with amphotericin B and additive activity with fluconazole
65
Q

What do Echinocandins treat?

A
  • Most species of Candida but not cryptococcus, trichosporon, and rhodotorula
66
Q

Examples of Echinocandins

A
  1. Anidulafungin
  2. Caspofungin
  3. Micafungin
67
Q

Side Effects of Echinocandins

A
  • fever
  • rash
  • nausea
  • phlebitis
  • histamine-like reaction (flushing)
    ** Overall well-tolerated
68
Q

Polyeyens

A
  • antifungal
  • antimicrobial polyene compounds target fungi
  • obtained from streptomyces bacteria
  • little is known about PK
  • bind and extract ergosterol directly from the cellular membrane of fungi
  • high protein binding (up to 95%)
  • primary route of elimination is unknown
69
Q

What do Polyeyens treat?

A
  • treats most Candida species
70
Q

Examples of Polyeyens

A
  1. Amphotericin B
  2. Nystatin
71
Q

Side Effects of Polyeyens

A
  • N/V
  • chills
  • rigors common
  • nephrotoxicity
  • electrolyte imbalances
72
Q

Pyrimidines

A
  • antifungal
  • combination therapy with amphotericin B for severe cryptococcal pneumonia, meningoencephalitis, and select invasive candida infections
  • interferes with DNA and protein synthesis
  • serum monitoring and renal dosing are necessary
73
Q

Examples of Pyrimidines

A
  1. Flucytosine (5-FC)
74
Q

Side Effects of Pyrimidines

A
  • hematologic toxicity
  • hepatic toxicity
  • GI toxicity
  • leukopenia
  • thrombocytopenia
75
Q

Misc. Antifungal Agents

A
  • inhibits fungal cell mitosis
  • deposited in karatin layer of skin, hair, nails
  • useful for dermaphyte infections (tinea capitus, cruris, pedis, unguium)
76
Q

Misc. Antifungal Agents Contraindications

A
  • hepatic failure
  • porphyria
  • pregnancy
77
Q

Examples of Misc. Antifungal Agents

A
  1. Griseofulvin
  2. Potassium iodide
78
Q

Side Effects of Misc. Antifungal Agents

A
  • hepatotoxicity
  • nephrosis
  • N/V/D
  • rash
  • photosensitivity
  • (PCN allergy)
79
Q

Mycobacterial Infections

A
  1. TB
  2. leprosy
  3. nontuberculosis mycobacteria (NTM)
80
Q

Antimycobacterial Agents

A
  • generally include multiple drug regimens and prolonged courses due to slow growth organisms
  • high rate of intrinsic resistance mutations and those that develop during treatment
  • typically 3-6 months of treatment required for drug susceptible TB
  • latent vs. active infection are treated differently
81
Q

Examples of Antimycobacterial Agents

A
  1. Antituberculosis agents
  2. Antimycobacterials (misc.)
82
Q

Antiviral Agents

A
  • viruses replicate within cells and often use host cells, enzymes, and other macromolecules to make viral particles
  • effective antivirals inhibit virus specific replication and/or inhibit virus directed protein synthesis
83
Q

What are viruses?

A
  • are microorganisms made up of single or double-stranded DNA or RNA in a protein coat (capsid)
84
Q

Examples of Antiviral Agents

A
  1. Adamantanes
  2. Antiretrovirals
  3. Interferons
  4. Monoclonal antibodies
  5. Neuroaminidase inhibitors
  6. Nucleosides and nucleotides
  7. HCV antivirals
  8. Antivirals (misc.)
85
Q

Examples of Protozoal Infections

A
  • Giardiasis
  • Trichomoniasis
  • Malaria
86
Q

Antiprotozoal Agents

A
  • used to treat infections caused by protozoa (single cell organisms) that act as parasites
  • protozoal infections often requires treatment using multiple drugs; vaccines are unavailable
  • many agents have potentially severe toxicity
87
Q

Examples of Antiprotozoal Agents

A
  1. Atovaquone
  2. Metronidazole
  3. Nitazoxamide
  4. Pentamidine
  5. Tinidazole
  6. Dapsone
  7. Amebicides
  8. Antimalarials
  9. Antiprotozoals (misc.)
88
Q

Side Effects of Antiprotozoal Agents

A
  • nausea
  • vomiting
  • disulfiram-like reaction
  • vaginitis
  • peripheral neuropathy
  • ataxia
  • confusion
89
Q

Clinical Pearls

A
  1. Confirm presence of infection
  2. Identify predisposing factors
  3. Identify the pathogen
  4. Collect infected material
  5. Perform gram stain
  6. Perform serologies
  7. Perform C & S
  8. Select empiric therapy considering every infected site
  9. Monitor therapeutic response
  10. Assess for therapeutic failure
  11. Assess host/drug factors

Pharmacology (6 decks)

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