Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacology for advance practice nursing 712 > Week 2 > Flashcards

Week 2 Flashcards

1
Q

Know the basic structure of bacteria.

A

a) BACTERIA / PROKARYOTES i) *include bacteria and archaea *singular: bacterium / plural: bacteria ii) PROPERTIES (1) Bacteria are the MOST NUMEROUS ORGANISMS ON EARTH. Organisms are classified as Bacteria by one characteristic: the lack of a cell nucleus (the name “prokaryote” means “before a nucleus”) iii) REPRODUCTION (1) Occurs by BINARY FISSION (mitosis) and CONJUGATION (exchange of DNA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Latin Prefixes

  • Cocci
  • Spirilla
  • Staph
  • Strep
A

Cocci - sphere
Bacilli - rods
Spirilla - spirals

Staph - in clusters

Strep - in chains

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Understand the concept of selective toxicity.

A

Toxic to microbes- harmless to host

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe the ways that selective toxicity occurs.

A
  • Disruption of bacterial cell wall
    • Unlike mammals, bacteria have a rigid cell wall with high concentration of solutes (High intracellular osmotic pressure)
  • Inhibition of an enzyme unique to bacteria
    • Sulfonamides inhibit transformation of PABA (para aminobenzoic acid) to folic acid
  • Disruption of bacterial protein synthesis
    • Mammalian and bacterial ribosomes are different.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Two ways of classification of antimicrobials.

A
  1. Classification by susceptible organism
  2. Classification by mechanism of action (MOA)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe the classification by susceptible organism.

A
  1. Antibacterial
  2. Antifungal
  3. Antiviral
  4. Narrow and Broad spectrum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe the classification by mechanism of action.

A
  1. Drugs work on:
    1. Cell wall synthesis or activate enzymes that disrupt cell wall
    2. Cell membrane permeability
      1. Leaky cell membranes
    3. Protein synthesis (lethal)
    4. Non-lethal inhibitors of protein synthesis
      1. Slows microbial growth
    5. Synthesis of nucleic acids
      1. Bind directly to nucleic acids or by interacting with enzymes required for nucleic acid synthesis
    6. Antimetabolites
      1. Disrupt specific reactions. Result in decrease synthesis of essential cell constituents OR nonfunctional constituents
    7. Viral enzyme inhibitors
      1. Inhibit specific enzymes required for viral replication and infectivity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Define the difference between bactericidial and bacteriostatic antimicrobials.

A
  1. Bactericidal: lethal to bacteria; kills the bacteria
  2. Bacteriostatic: slows down the bacteria growth; prevents the growth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Define the 4 mechanisms that microbes use to become resistant.

A
  • Decrease the concentration of a drug at its site of action
    • Cease active uptake or increase active export
  • Inactivate a drug
    • Produce drug metabolizing enzyme (penicillinase)
  • Alter the structure of drug target molecules
    • Drug receptors may change, resulting in decreased antimicrobial binding and action
  • Produce a drug antagonist
    • Microbes may synthesize compounds that antagonize actions (synthesis of increased quantities of PABA)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Explain strategies to decrease antibiotic resistance.

A
  • Natural Selection
    • Darwinian: Survival of the fittest
  • Mechanisms of Acquired Resistance
    • Spontaneous Mutation
    • Destruction/inactivation (Enzymatic)
    • Efflux
    • Genetic transfer
      • Conjugation
      • Transformation
      • Transduction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Does the microbe or the patient become resistant to antimicrobials?

A

The microbe becomes resistant NOT the patient!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Antibiotic use promotes resistance, but does not cause resistance, WHY?

A
  1. Microbes secrete compounds that are toxic to other microbes
  2. Microbes within a certain ecological niche compete for available nutrients
    1. Sensitive organisms are killed off thereby eliminating toxins they produce
    2. Killing sensitive organisms remove competition for nutrients
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Why is the correct diagnosis helpful to prevent drug-resistant microbe emergence?

A

Broad spectrum kills off more bacteria allowing for the infective bacteria to have more nutrients and continue to grow when other bacteria is killed off. Narrow spectrum is better which can be correctly determined by correct diagnosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe antibiotic use and drug-resistant microbe emergence.

A
  1. All antimicrobial drugs promote resistance- avoid when you can (DO NO HARM)
  2. Target disease NOT colonization
  3. Nosocomial infections
    1. Hospital acquired- exposure to multiple antibiotics- hardest to treat
    2. New Medicare Legislation: Avoiding antibiotic use in outpatient setting as much as possible
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Define Suprainfection- “Superinfection”.

A
  1. A new infection that occurs during the course of treatment for a primary infection
    1. Examples
      1. Antibiotics eliminate the inhibitory influence of normal flora
      2. Can be caused by drug resistant organisms
      3. Difficult to treat
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Define the differences between exogenous and endogenous infection.

A
  1. Endogenous infection: Disease originates within the body
    1. Alterations in normal flora
    2. Disruption of host defenses
  2. Exogenous infection: Disease originates outside the body
    1. Human to human
    2. Contact with bacterial populations
    3. Animals
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Define colonization.

A

The development of a bacterial infection on an individual, as demonstrated by a positive culture. The infected person may have no signs or symptoms of infection while still having the potential to infect others.

Do not treat colonization if not symptomatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Define Virulence.

A
  • Virulence refers to the pathogenicity/disease severity caused by the organism
    • Some have toxins or growth characteristics that avoid host immune response
    • Strep. Pyogenes- skin infection
    • Virulent but very susceptible to penicillin with little resistance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Understand significant Pharmacodynamics/MOA of antimicrobial classes

-Beta-Lactams: PCNs

A
  1. Pharmacodynamics
    1. Inhibit the biosynthesis of peptidoglycan bacterial cell wall
    2. Weaken the cell wall, causing bacteria to take up excess water and rupture (lyse) - Bacteriocidal
    3. Sensitivity
      1. Natural PCNs: Streptococcus, some Enterococcus strains, some non–penicillinase-producing Staphylococcus (gram positive)
      2. Aminopenicillins: greater activity against gram-negative bacteria because of enhanced ability to penetrate the outer-membrane organisms
      3. Combination with beta-lactamase inhibitors to broaden their spectrum: clavulanate, sulbactam, tazobactam
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Understand significant Pharmacodynamics/MOA of antimicrobial classes

-Beta-Lactams: Cephalosporins

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Understand significant Pharmacodynamics/MOA of antimicrobial classes

-Fluoroquinolones

A
  1. Pharmacodynamics: interfere with bacterial enzymes required for the synthesis of bacterial DNA
    1. Noted for extensive gram-negative activity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Understand significant Pharmacodynamics/MOA of antimicrobial classes

-Lincosamides: Clindamycin (Cleocin)

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Understand significant Pharmacodynamics/MOA of antimicrobial classes

-Macrolides and Azalides (Erythromycin, azithromycin, clarithromycin)

A
  1. Typically bacteriostatic but can be bactericidal
  2. Pharmacodynamics:
    1. Inhibits RNA-dependent protein synthesis
    2. Effective against gram + and gram –
    3. Variability amongst antimicrobials in the class
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Understand significant Pharmacodynamics/MOA of antimicrobial classes

-Tetracyclines

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Understand significant Pharmacodynamics/MOA of antimicrobial classes

-Glycopeptides

A
  1. Pharmacodynamics
    1. Vancomycin, telavancin (Vibativ), dalbavancin (Zeven)
    2. Used for severe gram-positive infections, such as MRSA resistant to first-line antibiotics
    3. Inhibits cell wall synthesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Understand sensitivity and clinical uses of antimicrobials

A
  1. Sensitivity
    1. Natural PCNs: Streptococcus, some Enterococcus strains, some non–penicillinase-producing Staphylococcus (gram positive)
    2. Aminopenicillins: greater activity against gram-negative bacteria because of enhanced ability to penetrate the outer-membrane organisms
    3. Combination with beta-lactamase inhibitors to broaden their spectrum: clavulanate, sulbactam, tazobactam
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Understand sensitivity and clinical uses of antimicrobials

-Beta-Lactams: Cephalosporins

A
  1. Clinical use and dosing
    1. Used for therapeutic failure in AOM
    2. First generation: streptococcal pharyngitis, skin infections
    3. Ceftriaxone: Gonorrhea
    4. Alternative for PCN allergic patients
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Understand sensitivity and clinical uses of antimicrobials

-Fluoroquinolones

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Understand sensitivity and clinical uses of antimicrobials

-Lincosamides: Clindamycin (Cleocin)

A
  1. Clinical use and dosing
    1. First-line therapy for MRSA in some areas
    2. Infections in PCN-allergic patients
    3. Drug-resistant Streptococcus pneumoneae infections
    4. Dental infections
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Understand sensitivity and clinical uses of antimicrobials

-Macrolides and Azalides (Erythromycin, azithromycin, clarithromycin)

A
  1. Clinical use and dosing
    1. Drug of choice for community-acquired pneumonia (mycoplasma)
    2. Chlamydia
    3. Pertussis
    4. Helicobacter Pylori infections (clarithromycin)
    5. Chronic bronchitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Understand sensitivity and clinical uses of antimicrobials

-Tetracyclines

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Understand sensitivity and clinical uses of antimicrobials

-Glycopeptides

A
  1. Clinical use and dosing
    1. Serious gram-positive infections resistant to other medications
    2. Oral vancomycin is used to treat C. difficile infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Understand significant pharmacokinetics of antimicrobials

-Beta-Lactams: PCNs

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Understand significant pharmacokinetics of antimicrobials

-Beta-Lactams: Cephalosporins

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Understand significant pharmacokinetics of antimicrobials

-Fluoroquinolones

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Understand significant pharmacokinetics of antimicrobials

-Lincosamides: Clindamycin (Cleocin)

A
  1. Pharmacokinetics:
    1. oral dosing completely absorbed; not affected by gastric acid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Understand significant pharmacokinetics of antimicrobials

-Macrolides and Azalides (Erythromycin, azithromycin, clarithromycin)

A
  1. Pharmacokinetics:
    1. well absorbed from duodenum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Understand significant pharmacokinetics of antimicrobials

-Tetracyclines

A
39
Q

Understand significant pharmacokinetics of antimicrobials

-Glycopeptides

A
  1. Pharmacokinetics
    1. Poor oral absorption, given IV
40
Q

Know significant side effects / adverse reactions associated with antimicrobial classes

-Beta-Lactams: PCNs

A
41
Q

Know significant side effects / adverse reactions associated with antimicrobial classes

-Beta-Lactams: Cepalosporins

A
42
Q

Know significant side effects / adverse reactions associated with antimicrobial classes

-Fluoroquinolones

A
43
Q

Know significant side effects / adverse reactions associated with antimicrobial classes

-Lincosamides: Clindamycin (Cleocin)

A
  1. ADRs:
    1. Black Box warning for severe colitis; dermatological: rash, burning, itching, erythema; transient eosinophilia, neutropenia, thrombocytopenia
44
Q

Know significant side effects / adverse reactions associated with antimicrobial classes

-Macrolides and Azalides (Erythromycin, azithromycin, clarithromycin)

A
  1. ADRs
    1. Dose-related GI: n/v, abdominal pain, cramping, diarrhea
    2. Skin: urticaria, bullous eruptions, eczema, Stevens-Johnson syndrome (erythromycin)
45
Q

Know significant side effects / adverse reactions associated with antimicrobial classes

-Tetracyclines

A
46
Q

Know significant side effects / adverse reactions associated with antimicrobial classes

-Glycopeptides

A
47
Q

Know significant drug interactions associated with antimicrobials

-Tetracyclines

A
48
Q

Know significant drug interactions associated with antimicrobials

-Beta-Lactams: Cephalosporins

A
49
Q

Know significant drug interactions associated with antimicrobials

A
50
Q

Know significant drug interactions associated with antimicrobials

A
51
Q

Know significant drug interactions associated with antimicrobials

-Macrolides and Azalides (Erythromycin, azithromycin, clarithromycin)

A
  1. Drug interactions
    1. Inhibitors of CYP3A4
52
Q

Know significant drug interactions associated with antimicrobials

A
53
Q

Know significant drug interactions associated with antimicrobials

A
54
Q

Understand recommendations for rational drug selection, monitoring, and patient education associated with antimicrobial classes

-Beta-Lactams: PCNs

A
55
Q

Understand recommendations for rational drug selection, monitoring, and patient education associated with antimicrobial classes

-Beta-Lactams: Cephalosporins

A
56
Q

Understand recommendations for rational drug selection, monitoring, and patient education associated with antimicrobial classes

-Fluoroquinolones

A
  1. Patient education
    1. Many drug interactions occur.
    2. Take with full glass of water.
    3. Drugs may cause dizziness.
    4. If tendon tenderness occurs, stop medication and notify provider.
57
Q

Understand recommendations for rational drug selection, monitoring, and patient education associated with antimicrobial classes

-Lincosamides: Clindamycin (Cleocin)

A
58
Q

Understand recommendations for rational drug selection, monitoring, and patient education associated with antimicrobial classes

-Macrolides and Azalides (Erythromycin, azithromycin, clarithromycin)

A
  1. Rational drug selection
    1. Often as alternatives for patients with PCN allergies
    2. Increasing resistance
  2. Monitoring
    1. For altered response to concurrent medications metabolized by CYP3A4 or CYP2C9
    2. Hepatic/renal impairment
    3. Hearing loss
  3. Patient education
    1. ADRs
    2. Drug interactions
    3. Dosing
      4.
59
Q

Understand recommendations for rational drug selection, monitoring, and patient education associated with antimicrobial classes

-Tetracyclines

A
  1. Rational drug selection
    1. Doxycycline and minocycline can be taken with food.
  2. Patient education
    1. Administration, ADRs, avoiding pregnancy
60
Q

Understand recommendations for rational drug selection, monitoring, and patient education associated with antimicrobial classes

-Glycopeptides

A
  1. Monitoring
    1. Hearing and renal function
  2. Patient education
    1. Administration
    2. ADRs
61
Q

Five Generations of Beta-Lactams: Cephalosporins

A
  1. First generation (cephalexin, cefazolin)
    1. Used for skin and soft tissue infections
    2. Primarily active against gram-positive bacteria, S. aureus and S. epidermidis and most streptococcus
  2. Second Generation / Cephamycins
    1. Second generation
      1. Same as first generation but BETTER coverage of H. influenza
      2. cefaclor
      3. cefprozil
      4. cefuroxime
    2. Cephamycins
      1. Unique – similar to first generation but some activity against anaerobes (B. fragilis)
      2. cefotetan
      3. cefoxitin
  3. Third generation (cefdinir, ceftriaxone…)
    1. Used for broader indications – oral and IV
    2. More active against gram-negative bacteria (less against gram +)
    3. Cefdinir and cefpodoxime have best gram + coverage
    4. Limited activity against anaerobes
  4. Fourth generation (cefepime IV only)
    1. Resistant to beta-lactamase
    2. Broader spectrum (gram + and gram -)
  5. Fifth generation
    1. Ceftaroline
    2. Similar to third generation, except active against methicillin-resistant S. aureus (MRSA)
62
Q

Classifications of Penicillins

A
63
Q

Groups of Fluoroquinolones

A
  1. OLDER GROUP
    1. ciprofloxacin (Cipro)
    2. norfloxacin (Noroxin)
    3. ofloxacin (Floxin)
  2. NEWER GROUP – RESPIRATORY QUINALONES (S. pneumoniae)
    1. levofloxacin (Levaquin)
    2. moxifloxacin (Avelox)
    3. delafloxacin (Baxdela)
64
Q

Understand significant pharmacodynamics/MOA of antimicrobial classes

-Sulfonamides, Trimethoprim, Nitrofurantoin

A
  1. Pharmacodynamics
    1. Sulfonamides block folic acid synthesis, trimethoprim inhibits DNA synthesis (sulfamethoxazole/trimethoprim)
    2. Usually bacteriostatic
    3. Nitrofurantoin inhibits protein synthesis / cell wall synthesis
    4. Inhibit both gram-positive and gram-negative bacteria
    5. E. coli, S. pyogenes, S. pneumoniae, H. influenzae, and some protozoa
    6. Resistance an issue
65
Q

Understand sensitivity and clinical uses of antimicrobials

-Sulfonamides, Trimethoprim, Nitrofurantoin

A
  1. Clinical use and dosing
    1. Most commonly used in UTI infections as a combined product or nitrofurantoin (empiric)
    2. MRSA is susceptible in some areas
66
Q

Understand significant pharmacokinetics of antimicrobials

-Sulfonamides, Trimethoprim, Nitrofurantoin

A
67
Q

Know significant side effects / adverse reactions associated with antimicrobial classes

-Sulfonamides, Trimethoprim, Nitrofurantoin

A
  1. ADRs:
    1. GI – anorexia, n/v, diarrhea, stomatitis; rashes (Stevens-Johnson syndrome, increased hypersensitivity reactions, photosensitivity;
    2. CNS – headache, dizziness, drug interactions Crystalluria
    3. Kernicterus – deposition of bilirubin in brains of newborns, sulfonamides displace bilirubin from plasma protiens
    4. DO NOT USE IN INFANTS LESS THAN 2 MONTHS AND PREGNANT WOMEN NEAR TERM (Sulfa)
    5. Avoid in glucose-6-phosphate dehydrogenase (G6PD) deficiency (Sulfa)
    6. Use cautiously in renal impairment
68
Q

Understand recommendations for rational drug selection, monitoring, and patient education associated with antimicrobial classes

-Sulfonamides, Trimethoprim, Nitrofurantoin

A
  1. Rational drug selection
    1. Low-cost alternative in children older than 2 months and in those with PCN allergies
  2. Patient education: finishing course, ADRs, resistance
    1. Drink plenty of water (2 L)
    2. Avoid sunlight and tanning beds
69
Q

Classifications of antifungals

-Allylamine

A
  1. Terbinafine (Lamisil), naftifine (Naftin), butenafine (Lotrimin Ultra, Mentax)
    1. Inhibits key enzyme to sterol biosynthesis causing cell death
    2. Used topically for treatment of dermatophytes
    3. Used orally for dermatophytes and onychomycosis
    4. Minimally absorbed from intact skin topically
70
Q

Classifications of antifungals

-Azoles

A
  1. Azoles
    1. Ketoconazole, fluconazole, posaconazole, voriconazole, itraconazole, miconazole, clotrimazole.
    2. Inhibit enzyme which results in inhibition of syntheses of cell membrane sterols resulting in a leaky cell membrane
    3. Cell death
    4. Wide spectrum including Candida species, cryptococcus, the endemic mycosis (blastomycosis, coccidiomycosis, histoplasmosis)
71
Q

Classifications of Antifungals

-Polyenes

A
  1. Polyenes
    1. Nystatin, Amphotericin B
    2. Effective against Candida infections
    3. Binds to sterols in the cell membranes of both fungal and human cells. When binds to sterol in fungal cell wall becomes leaky and allows for leakage of intracellular components
    4. Cell death
    5. Amphotericin B administered IV only
      1. Nephrotoxicity
      2. Stimulates release of proinflammatory cytokines resulting in fever, rigors, and chills
      3. Generally replaced by azoles
72
Q

Classifications of Antifungals

-Ethanolamines

A
  1. Ethanolamines
    1. Ciclopirox olamine (Loprox, Penlac Nail Laquer)
      1. Blocks transmembrane transport of amino acids into fungal cell.
      2. Dermatophytes (shampoo, cream, gel)
      3. Onychomycosis
73
Q

Classification of Antifungals

-Griseofulvin

A
  1. Griseofulvin
    1. Mitotic inhibitor – stops cell division
    2. Produced by a certain species of Penicillium
    3. Bone marrow suppression and liver damage
    4. Monitor CBC and liver functions
74
Q

Systemic Azoles and Other Antifungals

-Pharmacokinetics

A
  1. Absorption of itraconazole is enhanced by food.
  2. Absorption of griseofulvin is enhanced by fat.
  3. Fluconazole is an inhibitor of cytochrome 3A4 (CYP3A4) and CYP2C9.
  4. Itraconazole is an inhibitor of CYP3A4.
  5. Ketoconazole is an inhibitor of CYP3A4.
75
Q

Systemic Azoles and Other Antifungals

-ADRs

A
  1. All of the azoles and terbinafine have been associated with hepatotoxicity.
76
Q

Systemic Azoles and Other Antifungals

-Monitoring

A
  1. Monitor for efficacy
  2. Systemic antifungals
    1. Liver enzymes
    2. Griseofulvin: renal, liver, and complete blood count (CBC)
    3. Ketoconazole: liver function
    4. Itraconazole: liver function and electrolytes
    5. Terbinafine: liver enzymes and CBC
77
Q

Systemic Azoles and Other Antifungals

-Drug interactions

A
  1. Multiple because of CYP3A4 inhibition
78
Q

Systemic Azoles and Other Antifungals

-Clinical use and dosing

A
  1. Oral antifungals used to treat superficial infections caused by yeasts (Candida, pityriasis versicolor) and dermatophytes (tinea infections) and invasive systemic mycoses
  2. Fluconazole: requires loading dose
79
Q

Systemic Azoles and Other Antifungals

-Patient Education

A
  1. Patient education
    1. Instruct to take with food.
    2. Discourage alcohol use.
    3. Educate regarding signs of liver toxicity.
80
Q

Metronidazole, Nitazoxanide, and Tinidazole

-Pharmacoldynamics

A
  1. Metronidazole treats both parasitical and bacterial infections.
    1. Active against Trichomonas vaginalis, Entamoeba histolytica, Helicobacter pylori, Clostridium difficile
    2. Disrupts DNA and protein synthesis
  2. Nitazoxanide is used to treat Giardia lamblia and Cryptosporidium infections.
  3. Tinidazole is active against amebiasis, giardiasis, and trichomoniasis.
81
Q

Metronidazole, Nitazoxanide, and Tinidazole

-Pharmacokinetics

A
  1. Metronidazole is well absorbed when taken orally.
82
Q

Metronidazole, Nitazoxanide, and Tinidazole

-ADRs

A
  1. Metronidazole: anorexia, nausea, abdominal pain, dizziness, headache, metallic taste
  2. No ETOH while on metronidazole treatment
83
Q

Metronidazole, Nitazoxanide, and Tinidazole

-Clinical Use and Dosing

A
  1. Clinical use and dosing
    1. Metronidazole and tinidazole are used against the protozoal infections by T. vaginalis, G. lamblia, and E. histolytica.
    2. Metronidazole is used for anaerobic bacterial infections and bacterial vaginosis and is one of the drugs in H. pylori treatment.
84
Q

Metronidazole, Nitazoxanide, and Tinidazole

-Rational drug selection, monitoring, patient education

A
  1. Rational drug selection
    1. Metronidazole is on $4 retail lists.
    2. Avoid metronidazole in first trimester of pregnancy.
  2. Monitoring
    1. Resolution of symptoms
    2. Signs of leukopenia
  3. Patient education
    1. Administration
    2. Metallic taste with metronidazole
    3. Avoiding alcohol if taking metronidazole or tinidazole because of disulfiram-like reaction
    4. Concurrent treatment of partner if sexually transmitted infection is present
85
Q

Topical Antifungals: Precautions

A
  1. Topical
    1. Few contraindications because of minimal absorption
    2. Most are pregnancy category B
  2. ADRs
    1. Skin irritation, itching, burning, rash
  3. Drug interactions
    1. Few interactions with topical antifungals
    2. Theoretical interaction with azoles and amphotericin B
    3. Clotrimazole intravaginal preparations: should not be administered concurrently with nonoxynol-9 and octoxynol (contraceptive failure)
    4. Systemic antifungals: have a number of interactions
86
Q

Describe Fungi.

A
  • Very large and diverse group of microorganisms
  • Fungal infections also known as mycoses
  • Some fungi are part of the normal flora of the skin, mouth, intestines, vagina
  • Fungi are metabolically similar to mammalian cells and offer few pathogen specific targets
  • Dermatophyte – requires keratin to grow so are restricted to hair, nails, and superficial skin
  • Can be single cell or multicellular
  • Book differentiates dermatocytes from Candida species
87
Q

Describe the two types of Fungal/Mycotic Infections.

A
  1. Superficial
  2. Systemic*
    1. *Can be life threatening
    2. *Usually occur in immunocompromised host
88
Q

What topical antifungals are used for superficial fungal infections?

A
  1. Allylamines: terbinafine (Lamisil), naftafine (Nafta)
  2. Benzylamine: butenafine (Mentax)
  3. Imidazole (Azoles): clotrimazole, ketoconazole, miconazole, econazole, sertconazole, oxiconazole, sulconazole
  4. Polyene antifungals (Nystatin) – candida
  5. Ciclopirox (Penlac)
89
Q

What systemic antifungals are used for fungal infections of the skin?

A
  1. Griseofulvin
  2. Azoles (triazoles)
    1. Ketoconazole
    2. Itraconazole
    3. Fluconazole
  3. Terbinafine
90
Q

What systemic antifungals are used to treat systemic infection?

A
  1. Polyenes (macrocytic) – Amphotericin B (IV)
  2. Azoles
    1. Imidazole’s (primarily topical treatment)
    2. Triazoles – fluconazole, itraconazole, isavuconazole, posaconazole, voriconazole
  3. Allylamines
    1. Terbinifine
  4. Nuclear acid synthesis inhibitors
    1. Flucytosine (cryptococcosis)
  5. Grisiofulvan
91
Q

What are regular invasive fungi in fungal infections?

A
  1. Histoplasma casulatum
  2. Coccidiodes immitis
  3. Blastomyces dermatititis
92
Q

Fungal infections are opportunistic. True or False.

A

True

93
Q

Define opportunistic infections.

A

Infections that occur more often or are more severe in people with weakened immune systems than in people with healthy immune systems.

Pharmacology for advance practice nursing 712 (24 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions