Lecture 3 (ID)- Exam 2 Flashcards
1
Q
Cross tolerance:
* When does it happen?
* When switching to another opioid, what must happen with the starting dose of the new opioid?
A
- Development of tolerance to the effects of pharmacologically related drugs, particularly those that act on the same receptor site.
- When switching to another opioid, the starting dose of the new opioid must be reduced by at least 25% of the calculated equianalgesic dose to prevent overdosing
- Monitor clinical response and adverse effects
2
Q
What are ways to classify and group bacteria? (3)
A
- Aerobic/anaerobic
- Gram negative/positive
- Atypicals
2
Q
What are common gram negative bacteria (10)?
A
3
Q
What are the most common gram positive bacteria (10)?
A
4
Q
What are the gram + cocci?
A
- Staphylococcus spp (purple clumps)- aureus or epidermidis
- Streptococcus spp (purple chains)- viridian, pyogenes, pneumoniae
- Enterococcus spp
- Peptococcus
- Peptostreptococcus
Highlighted: anaerbic mouth flora
5
Q
What are the gram (-) cocci?
A
- Moraxella catarrhalis (common for URI)
- Neisseria spp (dicocci) -gonorrhea, meningitidis
6
Q
What are the gram + rods?
A
- Listeria
- Bacillus
- Corynebacterium
- Propionibacterium
- Clostridium spp-perfringens, difficile
7
Q
What are the gram - rods that are aerobes?
A
- Hemophilus Influenzae
- Escherichia Coli
- Proteus spp
- Klebsiella spp
- Pseudomonas spp
- Enterobacter spp
- Gardnerella vaginalis
- Legionella
- Pasteurella multocida
- Salmonella
- Shigella
- Campylobacter
- Yersinia
- Helicobacter
- Vibrio
- Bartonella
- Bordetella
8
Q
What are the gram - anaerobes?
A
- Bacteroides fragilis
- Fusobacterium spp
- Prevatella spp
9
Q
What are the atypical bacteria?
A
- Mycoplasma pneumoniae
- Chlamydia spp-pneumoniae, trachomatis
10
Q
What is the mycobacteria bacteria?
A
Tuberculosis
11
Q
What are the spirochetes bacteria?
A
- Treponema pallidum
- Borrelia burgdorferi
12
Q
What are the beta lactam antibiotics? (4) What type of agents are they?
A
Cell wall active agents
* Penicillins
* Cephalosporins
* Carbapenems
* Monobactams
13
Q
What are the glycopeptide antibiotics? What type of agent are they?
A
vancomycin-Cell wall active agent
14
Q
What is the MOA for penicillin?
A
Inhibits bacterial cell wall synthesis
* Target bacterial penicillin binding protein (PBP)
* Interfere with transpepiation
* Creates an unstable cell wall-> cell death
15
Q
- For penicillin, what needs to happen for renal impairment?
- What penicillin goes through hepatic elimination?
A
- Most required dose reduction for renal impairment
- Nafcillin – hepatic elimination
16
Q
What are the adverse effects? of penicillin
A
- GI effects: Nausea / vomiting / diarrhea
- Allergic reactions
17
Q
What are the penicillins? Aminopenicillins?
A
Penicillins
* Penicillin (IV, PO, IM)
Aminopenicillins
* Amoxicillin (PO)
* Ampicillin (IV)
18
Q
What are the Penicillinase Resistant (antistaphylococcal)? Extended spectrum (antipseudomonal)?
A
Penicillinase Resistant (antistaphylococcal)
* Oxacillin (IV)
* Nafcillin (IV)
* Dicloxacillin (PO)
Extended spectrum (antipseudomonal)
* Ticarcillin (IV)
* Piperacillin (IV)
19
Q
What are the b-lactamase combos?
A
- amoxicillin / clavulanate (Augmentin) (PO)
- ampicillin / sulbactam (Unasyn) (IV)
- piperacillin / tazobactam (Zosyn) (IV)
- ticarcillin / clavulanate (Timentin) (IV)
20
Q
Penicillin:
* What bacteria does penicillin treat (gram +, anaerobes and other)
A
- Gram (+): Steptococcus spp
- Anaerobe: Mouth flora-> Peptococcus and Peptostreptococcus
- Other: T. pallidum
21
Q
For ampicillin, amoxicillin, what bacteria do they treat (gram +, gram-, anerobe_?
A
- Gram(+): Streptococcus spp (same as PCN), listeria, enterococcus
- Gram (-): E. Coli, Proteus spp, H. influenzae, M. catarrhalis, N. meningitidis, Salmonella, Shigella, Helicobacter
- Anaerobe: Peptococcus and Peptostreptococcus (same as PCN)
22
Q
For oxacillin, nafcillin (methicillin), what bacteria do the meds treat?
A
- Streptococcus spp
- Staphylococcus spp but Not MRSA
Do not use methicillin because of renal toxity
23
Q
For Ticarcillin and Piperacillin, what bacteria do they treat (gram +, gram - and anaerobe)?
A
- Gram (+): Streptococcus spp (same as penicillin)
- Gram (-): same as ampicillin and amoxicillin Including Pseudomonas
- Anaerobe: B.fragilis
Amp and amox: E. Coli, Proteus spp, H. influenzae, M. catarrhalis, N. meningitidis, Salmonella, Shigella, Helicobacter
24
For Ampicillin/sulbactam and Amoxicillin/ clavulanat, what bacteria does it treat (gram +, Gram - and anaerobe?
* Gram (+): Staphylococcus, Streptococcus, Enterococcus
* Gram (-):Good vs most including B. Including beta-lactamase producing organisms
* Anaerobe: B. fagilis
## Footnote
* BROADEST
* beta lactamase inhibitors
25
For Ticarcillin / clavulanate and Piperacillin /tazobactam, what bacteria do they treat? (gram +, gram - and anaerobe)
* Gram (+): Staph, strept and enterococcus (Same as ampicillin / sulbactam)
* Gram (-): Good vs most including beta lactamase producing organisms and **Pseudomonas**
* Anaerobe: B. fragilis
## Footnote
* BROADEST
* B lactamase inhibitors
26
Cephalosporins:
* What is the MOA?
* What are the pharmokinetics?
* MOA: inhibits bacterial cell wall synthesis
* PK: most require adjustment for renal impairment; not **ceftriaxone**
27
What cephalosporin drug does not need to be adjusted for renal impairment ?
ceftriaxone
28
What are the adverse rxns of cephalosporins?
* Mild GI effects
* Rash
* Leukopenia (rare)
* PCN cross-reactivity
29
What are the 1st gen of cephalosporins?
* Cefazolin (Ancef) IV
* Cephalexin (Keflex) PO
| Fa+pha rule
30
What are the 2nd gen cephalosporins?
* Ce**fur**oxime (Zinacef-IV, Ceftin-PO)
* Cef**pro**zil (Cefzil) PO
* Cefote**tan** (Cefotan) IV
* Ce**fox**itin (Mefoxin) IV
| FURry FOXes TAN like PROs
31
What are the 3rd gen cephalosporins?
* Cefotaxime (Claforan) IV
* Ceftriaxone (Rocephin) IM/IV
* Cefpodoxime (Vantin) PO
* Cefdinir (Omnicef) PO
* Ceftazidime (Fortaz) IV
| -ime,-one, -ir
32
What is the 4th gen cephalosporin?
Cefepime (Maxipime) IV
33
What is the 5th gen cephalosporins?
Ceftaroline (MRSA)
34
What generations of cephalosporins are for anerobic activity?
1st and 2nd generation
35
For the cephalosporins, how do they treat gram + or -?
36
For first gen (Cefazolin (Ancef) IV and Cephalexin (Keflex) PO), what bacteria does the drugs treat? (gram pos, negative and anaerobe)
* Gram (+): Staphylococcus spp (not MRSA), Streptococcus spp (not Strep pneumoniae) and **Not Enterococcus spp**
* Gram (-): Moderate because better than PCN or ampicillin
* E. Coli
* Klebsiella spp
* Proteus spp
* Anaerobe: poor
37
For 2nd gen (Cefuroxime (Ceftin) PO Cefprozil (Cefzil) PO), what bacteria does the drugs treat? (gram pos, negative and anaerobe)
Gram (+): Staphylococcus spp (not MRSA), Streptococcus spp (not Strep pneumoniae) and **Not Enterococcus spp**
* SAME AS FIRST GEN
* Gram (-): Same as first (E. Coli, Klebsiella spp, Proteus spp) plus H.influenza and M.catarrhalis
* Anaerobe: Poor
38
What does 2nd gen (cefotetan and cefoxitin) treat?
Anaerobe: B. fragilis
39
For third gen,
* Cefotaxime
* Ceftriaxone (Rocephin) IV/IM
* Cefpodoxime (Vantin) PO
* Cefdinir (Omnicef) PO
* Cefixime (Suprax)
What do they treat? (gram pos, Gram neg and anerobes)
* Gram (+): Good Strep spp – including S. pneumoniae and Moderate Staph spp (MSSA)
* Gram (-): Good->N. gonorrhea
* Anaerobes: poor
40
What 3rd generation cephalosporin is great for pseudomonas?
Ceftazidime (Fortaz) IV plus limited staph/strep
41
For 4th gen, Cefepime(IV), what bacteria do they treat (gram pos, neg and anaerobes?
* What are they more of?
More resistant to beta lactamase
* Gram (+): good strep spp., moderate Staph spp but not MRSA
* Gram (-): Similar to ceftriaxone (n.gonorrhea)
* Anerobes: poor
42
What are the carbapenems?
Imipenem, meropenem, ertapenem, doripenem (IV only)->DEMI needs CARBs
| THE PENEMs!!!
43
What is the moa of carbapenems?
MOA: inhibit bacterial cell wall synthesis
* Still have beta-lactam ring but slight structure change including substitution from sulfur with carbon makes them more resistant to beta lactamases
44
Carbapenems:
* What type of antibiotic is it
* Which one does not cover pseudomonas or acinetobacter?
* What is doripenem approved for and not approved for?
* Very broad spectrum including most gram positives, gram negatives and anaerobes
* Ertapenem – does NOT cover Pseudomonas or Acinetobacter
* Doripenem
* Approved for complicated intra-abdominal and urinary tract infections only
* Not approved for the treatment of pneumonia (because it does not get into the lungs)
45
* Carbapenems should be reserved for what?
* What are the adverse reactions of carbapenems?
* Reserved for resistant infections only
ADR:
* Nausea / vomiting (worse with imipenem)
* Seizures (worse with imipenem)
46
Monobactam:
* What is the drug name?
* What is the MOA?
* What is the structure of the drug?
Aztreonam
* MOA: inhibit bacterial wall synthesis
* Beta-lactam ring is not fused – very resistant to beta lactamases
47
Aztreonam (monobactams):
* For are they great for? What activity do they not have?
* What are they reserved for?
* SE?
* Excellent gram-negative coverage including Pseudomonas spp
* **No gram-positive activity**
* Reserved for the treatment of resistant infections or patients with severe allergy to other beta lactam antibiotics
* Well tolerated with few side effects
48
PENICILLIN ALLERGY:
* Est. on how many ppl say they are allergic and how many actually are?
* What needs to be obtained with someone who reports pen allergy? Why?
* Estimated that 10% of the U.S. population labeled as penicillin allergic and < 1% actually are
* A detailed history should be obtained in patients who report a penicillin allergy
* Not an allergy – intolerance; correct chart
49
What are the delayed type rxns for pencillin allergies? Should you give them the med anyways?
Delayed-type reaction (e.g., Stevens Johnson Syndrome, Toxic Epidermal Necrolysis, serum-sickness, etc)
* Avoid penicillins, cephalosporins, carbapenems
50
What is a mild, without history of IgE mediated features or unverified patient, patient cannot recall reaction to penicillin getting? (recommended and considered)
Mild, without history of IgE mediated features or unverified (maculopapular rashes with or without pruritis, not hives), patient cannot recall reaction
* Minimal risk of IgE mediated reaction
* Recommend any generation cephalosporin or carbapenem
* Consider penicillin de-labeling with amoxicillin oral challenge
51
patients with past reaction with IgE medicated features should get what?
Past reaction with IgE medicated features (angioedema, anaphylaxis, wheezing, laryngeal edema, hypotension, hives/urticaria)
* Some risk of serious IgE mediated reaction
* Recommend:
52
What is the moa of vancomycin?
* MOA: inhibits bacterial wall synthesis
* Glycopeptide antibiotic – binds tetrapeptide chains and prevents linking
* Do not bind PBPs – bypass PBP mutations
* Resistance secondary to bacterial changes in the tetrapeptide chains – vancomycin can no longer bind
53
What are the indications of vancomycin?
* Treatment of gram-positive organisms resistant to other antibiotics
* Commonly incorporated into empiric regimens
* Treatment of Clostridium difficile enterocolitis
54
How do you give vancomycin and why?
Not absorbed from the GI tract – must be given IV for systemic infections
55
What are the adverse reactions to vancomycin?
* Ototoxicity
* Nephrotoxicity
* Thrombophlebitis
* “Red-man’s syndrome
56
# Vanco
Dose and frequency determined and monitored via what?
Via drug levels
* Troughs – adjust per clinical pharmacy
* Goal trough levels usually 15 to 20; depends on infection and MIC of bacteria
57
What are the different protein synthesis inhibitors?
58
What is the moa of aminoglycosides?
Inhibits bacterial protein synthesis
Irreversibly binds to 30s subunit and prevents protein synthesis
* Must enter through the cell wall to the nucleus
* Cannot penetrate the thick gram-positive cell wall
* Requires and oxygen-dependent co-transporter – not effective for anaerobic infections
59
What are the different aminoglycosides?
* Gentamicin
* Tobramycin
* Amikacin
* Streptomycin
60
For the aminoglycosides, what bacteria do they treat? (gram pos, neg, and other ones)
* Gram (+): Only in combination with cell active agent
* Strep spp, Entercoccus spp, Listeria
* Gram (-): Combination with cell active agents recommended
* Good against most including Pseudomonas spp
* Other: Anerobes are poor, and Mycobacteria TB, MAI best (amikacin, streptomycin)
## Footnote
Not staph gram (+), good gram (-), use with other drugs
61
What are the adverse effects of aminoglycosides?
* Ototoxix and Nephrotoxic
* Entirely renally eliminated; dose reduction required
* Contraindicated in pregnancy
* Monitoring: Drug levels and Serum creatinine
| GET LEVELS
62
Tetracyclines:
* What are the different drugs?
* What is the MOA?
Tetracycline, doxycycline, minocycline, tigecycline
MOA: inhibit bacterial protein synthesis
* Binds to A-site of 30S subunit
* Inhibits binding of tRNA to mRNA ribosome complex
63
Tetracyclines:
* What is the coverage?
* What is no longer used and why?
Broad spectrum gram-positive and gram-negative coverage
Parent drug (tetracycline) no longer used
* Less convenient dosing
* Less active
* More drug interactions
64
For doxycyline, what bacteria does it treat? (gram pos, neg and others?
65
What is the first line for tick borne diseases like rickettsia (RMSF) and borrelia (lyme)?
Doxycyclin
66
What are the adverse effects for tetracyclines?
* Phototoxicity
* Deposition in teeth – permanent yellow-grey-brown discoloration in children / fetus (worst with tetracycline)
* Nausea, vomiting, diarrhea -> do not take on empty stomach
* Erosive esophagitis (same as biphosphates)
* Minocycline – lupus like reaction
* Minocycline – pseudotumor cerebri-> increase intracranial pressure
* Tinnitus, vestibular symptoms (minocycline)-> dizzy and ringing of ears
67
What does american academy of pediatrics say about tetracyclines?
American Academy of Pediatrics (AAP) – doxycycline can be safely
administered for short durations (≤ 21 days) regardless of age
68
What are unique SE of minocyclines?
* lupus like reaction
* pseudotumor cerebri
69
What are the different macrolides?
Erythromycin, clarithromycin, azithromycin
70
What is the moa of macrolides?
* Inhibits bacterial protein synthesis
* Bind to 50s subunit and prevent translocation; ribosome can’t slide to the next codon on the mRNA
71
Macrolides:
* What is the coverage?
* What drug is not used a lot and why?
Broad spectrum gram-positive and gram-negative coverage
Parent drug (erythromycin) minimal use as antimicrobial
* Less convenient dosing
* More adverse effects
* More drug interactions
72
For Erythromycin (PO, IV), Azithromycin (PO, IV) Clarithromycin (PO), what bacteria does it treat (gram pos, neg and others)?
73
What are the interactions of macrolides?
Avoid concomitant administration with magnesium or aluminum-
containing antacids
74
What are the adverse reactions of macrolides?
GI: nausea, vomitingE, diarrhea
* Erythromycin > clarithromycin > azithromycin
Prolongation of QTc – interval
* Avoid in patients with known prolonged QT or history of arrythmias
* Caution with other drugs that prolong QTc interval
Hepatotoxicity
Drug interactions CYP3A4 (erythromycin, clarithromycin)
Hearing loss (erythromycin)
75
What macrolides has the most SE?
Erythromycin
76
Clindamycin:
* What is the MOA?
* What does it inhibit in vitro
MOA
* Inhibits bacterial protein synthesis
* Bind to 50s subunit and prevent translocation; ribosome can’t slide to the next codon on the mRNA
Inhibits in vitro the production of the streptococcus superantigen pyrogenic exotoxins A (SPEA) and B (SPEB)-> used with cell wall active agent to neutralize the endotoxin (toxic shock)
77
For clindamycin, what bacteria does it treat? (gram pos, neg and anaerobes)
78
linezolid:
* What is the MOA?
* Inhibits bacterial protein synthesis
* Bind to 50s subunit and prevents it from binding to the 30S subunit to form initiation complex; stops protein synthesis before it begins
79
What are the SE of linezoid?
* Nausea, vomiting, diarrhea, rash – short term
* Bone marrow suppression (leukocytopenia, thrombocytopenia)
* Peripheral neuropathy and optic neuropathy – long term
* Inhibits monoamine oxidase – may interact with other medications that increase serotonin (MAOIs, SSRIs, SNRIs)
* Serotonin syndrome – fever, agitation, mental status changes, muscle rigidity, tremor, seizures
80
What drug can cause serotonin syndrome when taken with a monoamine oxidase drugs?
Linezolid
81
For linezolid, what bacteria can be treated? (gram pos, neg and others)
* Gram (+): Excellent; including MRSA and VRE
* Used in locations where MRSA cannot be penetrated
* Gram (-): poor
* Other: poor
82
What are the different DNA synthesis inhibitors?
83
Fluoroquinolones:
* What are the different drugs?
Ciprofloxacin, levofloxacin, moxifloxacin, delafloxacin
84
Fluoroquinolones:
* What is the MOA?
* What is it metabolized via what?
* Should not be taken with what and why?
* Inhibits bacterial replication by inhibition of DNA gyrase (topoisomerase I) and topoisomerase IV)
* Metabolized via CYP450; also inhibitor
* Many drug interactions
* Should not be taken with calcium, iron, zinc – bind quinolones and cause chelation and decreased absorption
85
Fluoroquinolones:
What are the adverse effects?
* Tendonitis – achilles tendon MC (avoid in athletes or elderly)
* Cartilage damage
* GI distress
* CNS headache, agitation **dizziness**, insomnia, peripheral neuropathy, seizures
* Prolong QT interval: monitor QTc in patients on concomitant drugs that prolong QT interval
* **Hyper / hypoglycemia (MC moxifloxacin)**
## Footnote
Need to be careful with elderly
86
For ciprofloxacin, levofloxacin, and moxifloxacin, what bacteria can be treated (gram pos, neg and anaerobe)?
87
For delafloxacin, what bacteria does it treat? (gram pos, neg and anaerobe)
Gram (+): s. aureus including MRSA
Gram (-): Excellent including Pseudomonas (ciprofloxacin superior)
Anaerobe: Moderate including b.fragilis
88
What is the black box warning for fluoroquinolones?
* Serious, potentially irreversible adverse effects including tendinopathy and CNS effects. Avoid use / discontinue in any patients experiencing these side effects.
* Risks > benefits for chronic bronchitis, sinusitis, uncomplicated cystitis
89
What is the MOA of metronidazole?
inhibits DNA synthesis; produces free radicals which damage bacterial DNA; bacteria cannot produce nucleic acids
90
What are the adverse effects of metronidazole
* Anorexia
* Nausea
* Stomach cramps
* Disulfiram-like effect (nausea, vomiting and headaches if taken with alcohol-> 24hr to 48hrs)
91
For metronidazole, what bacteria does it treat (Gram pos, neg and others)?
* Gram (+): poor
* Gram (-): poor, H.Pylori (in combination)
* Anerobic: Bacteroides fragilis and Clostridium difficile
* Other: Entamoeba histolytica, Gardnerella spp, Trichomonas
* Giardia
92
Sulfamethoxazole/trimethoprim (SMX/TMP):
* What is the MOA?
inhibit bacterial DNA synthesis; each inhibit different steps in bacterial folate synthesis; **no folate = no nucleic acids = no DNA**
93
Sulfamethoxazole/trimethoprim (SMX/TMP):
* Dosing based on what?
* What is the strength dose?
* What can happen if Allergic reaction to sulfonamide group?
* Dosing based on TMP component
* One double strength tablet = 160 mg TMP/ 800mg SMX
* Allergic reaction to sulfonamide group: can cross react with other drugs with sulfonamide group including hydrochlorothiazide and glyburide
94
# ⭐️
Sulfamethoxazole/trimethoprim (SMX/TMP):
* What is the CI?
* What type of inhibitor? what does this cause?
* CI: pregnancy, infants < 2 months dt leukopenia and binds to albumin and kicks off billy rubin
* CYP450 2C9 inhibitor - increases warfarin levels
95
Sulfamethoxazole/trimethoprim (SMX/TMP):
* What are the adverse effects?
* Nausea, vomiting
* Skin rash, photosensitivity, erythema multiforme, Stevens-Johnson syndrome
* Bone marrow suppression
* Hemolytic anemia – patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency
* Crystalluria / nephritis
* Kernicterus in neonates
96
For Sulfamethoxazole / trimethoprim (Bactrim / Septra), what bacteria does it treat (gram pos, neg and other)?
* Gram (+): staph spp including MRSA
* Gram (-): good versus most, not pseudomonas
* Other: poor anaerobic and DOC for pneumocystis jirovecii
97
What is the DOC for Pneumocystis jirovecii
Sulfamethoxazole / trimethoprim (Bactrim / Septra) (IV/PO)
98
Rifampin:
* What is the MOA?
* Never use as what?
* Inducer of what?
* MOA: inhibits bacterial RNA synthesis; inhibits RNA polymerase
* NEVER us as monotherapy – rapid development of resistance
* Inducer of CYP3A4 – many significant drug interactions * Monitor closely
99
What are the adverse effects of rifampin?
* Nausea, vomiting, diarrhea
* Red-orange discoloration of tears, sweat, urine, etc-> any body fluid
* Stains contact lenses
* Flu-like syndrome – rash, fever, abdominal pain
* Hepatitis – rare but can be life-threatening
100
For rifampin, what bacteria does it treat? (gram pos, neg and other)
* Gram (+): Staph and Strep spp including MRSA
* Gram (-): Poor->H. influenzae, N. Meningitidis (post exposure prophylaxi)
* Other: M.tuberculosis
101
Daptomycin:
* What is the MOA?
binds to and depolarizes the bacterial cell wall membrane; intracellular inhibition of DNA, RNA, and protein synthesis
102
* What is the pharmokinetics of daptomycin? What is it not recommended for?
* What does it penetrate?
PK: not absorbed orally, 90% protein bound, 80% eliminated unchanged in the urine
* Pulmonary surfactant inactivates daptomycin not recommended for treatment of pneumonia
Penetrates biofilm of gram-positive organisms
103
What are the adverse effect of daptomycin?
Myopathy and rhabdomyolysis
* Monitor weekly creatine phosphokinase (CPK); more frequent with renal failure or patients on statins
* Eosinophilic pneumonia
* Peripheral neuropathy
104
For daptomycin, what bacteria does it treat (gram pos, neg and others)?
* Gram (+): Excellent including MRSA and VRE
* Gram (-): none
* Anaerobe: none
105
# Mechanism of resistance
What happens when there is an antibioic modification or inactivation?
* Bacteria develop enzymes that inactivate and destroy antibiotics
* E.g. – beta lactamase destroys beta lactam ring
106
# Mechanism of resistance
What happens when there is Alteration of target or binding site – antibiotic can’t bind to target
E.g. – MRSA modifies its penicillin binding proteins
107
# Mechanism of resistance
what happens when there is a bypassing metabolic inhibition?
E.g., sulfonamides inhibit folic acid synthesis; bacteria find ways to scavenge folic acid from the environment
108
What happens when there is a prevention antibiotic accumulation – decrease intra- bacteria abx conc
E.g., preventing cell membrane permeation, creation of efflux pumps
109
What are the different antimicrobial resistance mechanisms?
110
What is a bactericidal antibiotics? What are the examples?
Antibiotics that kill bacteria without help from patient’s immune system
* Penicillins
* Cephalosporins
* Carbapenems
* Vancomycin
* Fluoroquinolones
* Daptomycin
* Metronidazole
* Sulfamethoxazole/trimethoprim
111
Are bacteriostatic drugs? what are the examples?
Antibiotics that inhibit the growth of bacteria – utilize the patient’s immune system to kill the bacteria
* Tetracyclines
* Clindamycin
* Macrolides
* Linezolid
112
What are some caveats about bacteriostatic and bactericidal drugs?
* Some drugs are static at low concentrations and cidal at high concentrations
* Some drugs are static against certain bacteria and cidal against others
* Some drugs are static on their own but cidal when combined with other antibiotics
113
When is bactericidal necessary?
* Patient’s immune system is not functioning
* Serious infections that require early bacterial killing to preserve life or function (sepsis, meningitis)
* Site of infection is poorly accessible to antibiotics
114
When is bacteriostatic appropriate?
* Antibiotic targets a specific bacteria
* Only drug available to treat a specific bacteria due to resistance
* When it is used with another drug for synergistic effects
115
116
What are imidazoles? What are triazoles?
* Imidazoles: Clotrimazole, Miconazole and Ketoconazole
* Triazoles: Itraconazole, Fluconazole, Voriconazole, Posaconazole, Isavuconazole
117
* For clostrimazole and micronazole, what is the MOA, route and SE?
* Ketoconazole?
118
For the triazoles: What is the MOA, route and SE?
119
What does fluconazole treat?
120
What does itraconazole treat?
3c's
121
For Voriconazole, Posaconazole,Isavuconacole what do they treat?
122
Echinocandins:
* What is the spectrum of activity?
* Candida spp = +++
* Aspergillosis = ++
123
# Echinocandins
For caspofungin, micafungin and anidulafungin, what is the MOA, route and SE?
124
Nystatin:
* What is the fungals treated, MOA, Route and SE?
Candida only
* MoA: Increases cell permeability causing cell death
* Route: topical/PO-> diapers or for thrush and diapers
* SE: GI distress
125
Amphotericin:
* What are the fungals that can be treated, MOA, route and SE?
126
Flucytosine:
* What fungals can be treated, MOA, Route and SE?
127
Acyclovir:
* Pharmcokinetics, MOA, Spectrum and SE?
128
Valacyclovir:
* PK, MOA, Spectrum and SE?
129
For Famciclovir (PO), Ganciclovir (IV) and valganciclovir (PO):
* What is the MOA, spectrum and SE?
130
131
What anti-influenza agents are M2 channel blockers, neuraminidase inhibitors, and endonuclease inhibitors?
* M2: Amandtadine and rimantidine
* Neuraminidase inhibitors: Oseltamivir and zanamivir
* endonucleases inhibitor: Baloxavir marboxil
132
Amantadine and rimantidine:
* What is the MOA, Spectrum and SE?
133
For Oseltamivir and Zanamivir, what is the MOA, spectrum and SE?
134
For Baloxavir marboxil (Xofluxa), what is the MOA, spectrum and SE?
135
Neuraminidase inhibitors MC:
* What drug is approved for all age groups including preg woman?
Oseltamivir MC
* oral tablets and suspension
136
What diseases should you have Treatment and post-exposure prophylaxis for influenza?
* Chronic lung disease (COPD, asthma)
* Organ dysfunction (heart, kidney, liver)
* Neurologic disorders
* Immunocompromised
* Obese
* Extremes of age (> 65 years or < 2 years)
* Pregnancy
137
* For the anti-influenza agents, when must treatment start?
* Hospitalized patients may benefit if started when?
* What is the effect of starting meds early?
* Treatment must start within 48 hours of symptoms onset – modest symptom reduction in healthy patients
* Hospitalized patients may benefit if started within 5 days of symptom onset
* Decrease in duration of symptoms (avg: 1 day) and severity of disease
138
What si the recommendion for seasonal vaccine?
Seasonal vaccine recommended for all patients > 6 months of age without vaccine contraindications
139
antimicrobial selection:
* what do you need to confirm?
* What do you need to identify?
* What do you need to start?
140
For empiric therapy, what are the patient factors?
141
For empiric therapy, what are the drug factors?
142
What is a culture and sensitivity?
143
When it comes to monitoring, what are things that you need to do or look for?
144
When should you convert IV to PO?
145
