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NURS 572 > Week 2 Chapter 24 > Flashcards

Week 2 Chapter 24 Flashcards

1
Q

Antimicrobial resistance is mediated through what major categories of cellular processes?

A
  1. production and excretion of an enzyme that hydrolyzes the antimicrobial
  2. genetic alteration of the microbial site where the antimicrobial binds
  3. alteration in cellular membrane proteins that prevents antimicrobial from penetrating
  4. transmembrane efflux pumps that transport antimicrobials out
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2
Q

What antibiotics are in the beta-lactam super class?

A
  1. penicillins
  2. cephalosporins
  3. carbapenems
  4. monobactams
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3
Q

What is the active moiety of the beta lactic class?

A

a four member ring known as the beta lactic ring.

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4
Q

Mechanism of action of the beta lactam ring?

A

inhibits the biosynthesis of the bacterial cell wall, specifically the peptidoglycan structure

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5
Q

What are the three bacterial enzymes that the beta lactam ring binds to?

A
  1. transpeptidase
  2. carboxypeptidase
  3. endopeptidase
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6
Q

What is the minimum inhibitory concentration? (MIC)

A

when the beta lactam drug concentration exceeds the MIC of the pathogen by 40-50% of the dosing interval, that is when vitro efficacy is maximized

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7
Q

What are the chemical characteristic of penicillin and the 4 penicillin subclasses?

A

attached of different chemical components to 6-aminopenicillins acids results in different penicillin subclasses.
1. natural penicillins
2. aminopenicillins
3. antistaphylococcal penicillins
4. antipseudomonal or extended-spectrum penicillins

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8
Q

What are the 4 natural penicillins?

A
  1. Penicillin V - oral
  2. Procain penicillin - IM
  3. Benzathine penicillin - IM
  4. Penicillin G - IV
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9
Q

What are natural penicillins active against?

A

aerobic, gram positive organisms
1. strep - such as strep pneumoniae and group A beta hemolytic strep. group A and B strep
2. some enterococcus strains
3. some non-penicillinase producing staph

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10
Q

Staph A and natural penicillin resistance

A

only 5-15% of community acquired staph A are susceptible to natural penicillin, the vast majority excretes an enzyme called penicillinase

penicillinase hydrolyzes that beta lactam ring making it ineffective

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11
Q

Penicillin resistance strep pneumoniae and their prevalence

A

has decreased prevalence due to less natural penicillin usage and wifespread vaccination for strep pneumoniae

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12
Q

What is penicillin G reliable for?

A

treating listeria monocytogenes but no longer for gonorrhoeae or staph species

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13
Q

What is amino penicillin reliable for?

A
  1. gram positive organisms - such as strep and enterococcus species
  2. methicillin susceptible staph A (MSSA)

greater activist against gram negative bacteria because of their enhanced ability to penetrate the outer cell membrane

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14
Q

What are two drugs that are in the subclass amino penicillin?

A
  1. ampicillin
  2. amoxicillin
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15
Q

What are ampicillin and amoxicillin combined with for enhanced gram negative and anaerobic activity?

A

beta lactase inhibitors called clavulanic acid and sulbactam

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16
Q

Antistaphylococcal penicillins subclass consists of

A
  1. nafcillin - IV
  2. oxacillin - IV
  3. dicloxcillin - PO
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17
Q

MOA of antistaphycoccal penicillin and what is it effective against?

A

chemical modifications made this class more stable in the presence of penicillinase produced by staph but makes it ineffective in treating enterococcus and gram negative species

effective against
1. strep, MSSA

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18
Q

What are the drugs that are in the subclass antipseudomonal penicillins?

A
  1. pipperacillin and a beta lactase inhibitor tazobactam
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19
Q

MOA of antipseudomonal penicillins

A

has enhanced activity against gram negative bacilli such as: E coli, Klebsiella, Pseudomonas aeruginosa, and enterobacter and proteus mirabilis

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20
Q

Penicillin precaution and contraindication

A
  1. serious hypersensitivity reactions
  2. atopic skin conditions
  3. type 1 allergic reactions to cephalosporins, carbapenems, or betalactamase inhibitors
  4. piperacillins may cause hemorrhagic manifestations, use in cautions with anemic or bone barrow depression patients
  5. use in caution with breastdfeeding patients due to it passing to milk and to undeveloped infant kidneys
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21
Q

Adverse reactions of penicillins

A
  1. type I hypersensitivity reactions - tachycardia, dyspnea, diaphoresis, loss of consciousness, circulatory collapse
  2. a pruritic maculopapular rash (not true allergy)
  3. other hypersensitivity reactions - skin rashes, serum sickness like reaction (joint pain, fever), blood dyscrasia
  4. common adverse reactions - GI symptoms
  5. hepatotoxicity in penicillinase resistance penicillins
  6. broad spectrum or prolonged used can cause bacterial or fungal overgrowth such as C. dif
  7. nephrotoxicity
  8. Penicillin G - mental disturbances
  9. irritability and seizures in renal insufficiency patients
  10. platelet aggravation in piperacillin
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22
Q

Drug interactions with penicillins are

A
  1. oral contraceptives - decreases OC efficacy by alternating serum levels of estrogen
  2. food and acidic juices - decreases oral absorption of penicillin V and penicillinase resistance penicillins
  3. lasix - hypokalemia
  4. methotrexate - increases methotrexate levels
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23
Q

Clinical use for penicillins

A
  1. respiratory infections
  2. PNA
  3. STIs
  4. UTIs
  5. wound infections
  6. endocarditis prophylaxis
  7. H pylori
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24
Q

Steps for antimicrobial drug selection

A
  1. clinical diagnosis
  2. obtains cultures and/or specimens
  3. microbial diagnosis/results
  4. select drug results from sensitivity or usual susceptibility
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25
Q

Factors the contribute to antimicrobial resistance are

A
  1. increase in populations of immunocompromised patients
  2. number and complexity of invasive procedures
  3. use (inappropriate and appropriate) of antimicrobials
  4. survival of patients with chronic diseases
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26
Q

What is the purpose of the antibiotic stewardship program?

A

promote appropriate antimicrobial use, promote avoidance of antimicrobials when not indicated, includes treatment pathways for specific infectious diseases

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27
Q

When are antimicrobials indicated?

A
  1. when the benefits of therapy outweighs the cost and risk of treatment
  2. for self limiting infections (self recovering) infections, treat symptoms only, no antibiotics needed
  3. if antibiotic use is needed, empirical selection or definitive, suture derived selections are appropriate strategies
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28
Q

What are cephalosporins?

A
  • beta lactam antibiotics and are chemically and structurally related to the penicillins
  • divided into 5 generations
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29
Q

MOA of cephalosporins

A
  • inhibits mucopeptide synthesis in bacterial cell wall, making the bacterium osmotically unstable
  • inhibits PBPs involved in cross linking peptidoglycan in the cell wall
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30
Q

First generation cephalosporins are active against?

A
  • gram positive cocci and most strep
  • enterobacterales isolated in the community - E coli, proteus mirabilis, kleb pneumoniae
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31
Q

First gen cephalosporins are resistance against?

A
  • enterococcus
  • enterobacterales isolated in hospital settings
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32
Q

Drugs that are in the first gen cephalosporins are?

A
  • cephalexin
  • cefadroxil
  • cefazolin - IV only
  • do not readily enter the CSF
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33
Q

Drugs that are in the second gen cephalosporins are?

A
  • cefaclor
  • cefprozil
  • cefuroxime
  • cefotetan
  • cefoxitin
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34
Q

Second gen cephalosporins are active against?

A
  • same as first gen
  • increased activity against H influenzae
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35
Q

Second gen cephalosporins are resistance to?

A
  • anaerobes
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36
Q

Third gen cephalosporins drugs includes?

A
  • cefdinir
  • cefpodoxime
  • ceftriaxone
  • ceftazidime
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37
Q

Third gen cephalosporins are active against?

A
  • strep species
  • gram positive bacteria
  • ceftazidime - reduced gram positive potency but has increased gram negative activity to pseudomonas aeruginosa
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38
Q

Third gen cephalosporins are resistance for

A
  • anaerobes
  • historically used for uncommon gram negative but now discouraged
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39
Q

Fourth and fifth gen and nongenerational cephalosporins drugs includes

A

4th - cefepime
5th - ceftaroline
non generational - ceftolozane/tazobactam and ceftazidime/avibactam

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40
Q

What are the mechanisms of resistance in cephalosporins?

A
  • beta lactamase production and altered target sites (changes in PBPs that prevents all cephs from binding to receptors)
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41
Q

Precaution and contraindications for cephalosporins are

A
  1. hypersensitivity (type 1)
  2. renal function impairment
  3. safe in prego but should consider risk v benefits
  4. excreted in breastmilk
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42
Q

ADR for cephalosporins are?

A
  1. type 1 hypersensitivity reactions
  2. type 3 delayed hypersensitivity
  3. parental administration - seizure in presence of renal impairment
  4. coagulation abnormalities
  5. immune hemolytic anemia
  6. cliff
  7. acute liver injury, bloody diarrhea, pulmonary infiltrates, biliary sludge
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43
Q

Drug interactions with cephalosporins are?

A
  1. loop diuretics - increased risk for neurotoxicity
  2. warfarin - increased bleeding
  3. probenecid - increased ceph levels by competitively inhibiting renal tubular secretion
  4. alcohol - acute disulfiram like reaction
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44
Q

Clinical use for cephalosporins are

A
  1. respiratory pathogens
  2. otitis media
  3. sinusitis
  4. group A strep pharyngitis
  5. PNA
  6. chronic bronchitis
  7. UTIs
  8. ceftriaxone IM - gonorrhea
  9. 1st gen ceph - staph skin infections
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45
Q

What are fluoroquinolones?

A

synthetic, broad spectrum antibiotics chemically related to quinolone nalidixic acid

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46
Q

What drugs are part of the fluoroquinolones?

A

Older group - cirpfloxacin and ofloxacin
New group - Levofloxacin, moxifloxacin, and delafloxacin
ophthalmic solution - gatifloxacin

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47
Q

MOA of fluoroquinolones

A
  1. inference with enzymes required for the synthesis and repair of bacterial DNA
  2. Fluorine molecule - increased potency against gram negative organisms and broadens the spectrum to include gram positives as well
  3. piperazine moiety - responsible for the antipseudomonal activity of the antibiotic
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48
Q

Which medication of the flouroquinolones has a broader gram positive spectrum and is a pure I-isomer of racemic ofloxacin?

A

Levofloxacin

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49
Q

How does fluoroquinolones interfere with the bacteria’s DNA?

A
  1. inhibits bacterial topoisomerase II and IV
  2. inhibiting topoisomerase II prevents the relaxation of positively supercoiled DNA that is required for replication and IV interferes with separation of replicated DNA into the daughter cells during replication
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50
Q

Fluoroquinolones are active against?

A
  1. gram negative activity
  2. some gram positives
  3. only newer ones are active against staph E. and strep
  4. chlamydia
  5. mycobacterium
  6. moxifloxacin - anaerobic organisms
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51
Q

What are fluoroquinolones resistance against?

A
  1. resistance is caused by mutations in the quinolone-binding region or by a change in the permeability of the organism
  2. there is already resistance for gonorrhea and use for empirically intra abdominal infection because of E. coli resistance, and TB resistance
  3. should be received for use only when other alternatives are hazardous
51
Q

Precaution and contraindications in fluoroquinolones are

A

BOX WARNING - risk of tendon rupture and tendonitis and avoid all fluroquinolones in patients with MS
1. avoided in diseases in which less toxic alternatives are available - acute bacterial sinusitis, acute exacerbations of chronic bronchitis, uncomplicated UTIs
2. has increased risk for aortic dissection or aneurysms
3. causes prolonged QTc if combined with other prolonged QTc drugs
4. use in caution with renal impairments
5. CNS stimulant due to fluoroquinolones inhibiting bonding of GABA to its receptors therefore patients with seizures and CNS disorders should use with caution
5. patients on dialysis has high risk for tendon rupture and adverse CNS reactions
6. liver failure patients - monitor for jaundice
7. avoid in prego unless benefits justifies the risk
8. excreted in breast milk, use only if there are no other alternatives
9. should not used age 18 and under due to arthropathy and osteochondrosis

52
Q

ADR of fluoroquinolones

A
  1. cdiff
  2. common GI reactions and altered taste
  3. steven johnson syndrome and first dose hypersensitivity and anaphylaxis
  4. phototoxicty
  5. superinfections with repeated use
  6. cardiovascular - angina, MI, a flutter, ventricular ectopy, cerebral thrombosis
  7. CNS symptoms
  8. fluctuations in blood sugars
  9. ARF and crystalluria
  10. tendonitis
53
Q

Drug interactions with fluoroquinolones are

A
  1. weakly inhibit drug metabolism by cytochrome P450 CYP 3A4 which increases levels of caffeine, zolpidem, olanzpaine and clozapine
  2. warfarin has increased effects
  3. dairy reduces the absorption or cipro
  4. antacids, iron salts, sevelamer, sucralfate, and zinc salts prevents absorption of antibiotic
54
Q

Clinical usage for fluoroquinolones are

A
  1. community acquired PNA
  2. UTIs but use alternatives first
  3. second line treatment for chlamydia and epididymitis
  4. first line defense for travelers diarrhea and severe diarrhea not associated with antibiotic therapy
  5. bone and joint infections
  6. first line defense for typhoid fever
  7. can be used as chenophophylaxis
55
Q

MOA of clindamycin

A
  1. binds to the 50S subunit of the bacterial ribosome and suppresses protein synthesis
56
Q

What is clindamycin active against?

A
  1. gram positive and selected anaerobic pathogens
57
Q

What is clindamycin resistant against?

A
  1. mechanism of resistance include mutation or modification of the ribosomal receptor site and enzymatic inactivation of clindamycin
  2. not effective against enterococci and gran negative aerobic organisms
58
Q

Clindamycin precaution and contraindications

A
  1. can be used cautionary in prego cause it crosses placenta
  2. can be used cautionary in breastfeeding cause it goes into breastmilk
  3. can be used in infants and children but with serious infections only
59
Q

ADR in clindamycin

A
  1. most common are GI related
  2. bitter metalic taste
  3. cliff
  4. dizziness, vertigo, headache, hypotension, cardiac arrhythmias
60
Q

Clinical use for clindamycin are

A
  1. first line therapy for MRSA in populations of low resistance (pediatrics)
  2. second line treatment for gram positive cocci
  3. use in penicillin allergic patients for bacterial endocarditis prophylaxis, pneumococcal PNA, skin and tissue infections
  4. S pneumoniae
  5. second and third line of defense for upper and lower respiratory infections
  6. first line defense for odontogenic infections
  7. used for pregnant women and children for malaria and other protozoal infections if not able to take the alternatives
61
Q

What are macrolide and azalides?

A
  1. macrolides are compounds characterized by a macrocyclic lactone ring with deoxygenated sugars attached
  2. azalides are derived from erythromycin by the addition of a methylated nitrogen to the lactone ring
62
Q

What drugs are macrolides and what drugs are azalides?

A

macrolides - erythromycin, clarithromycin
azalides - azithromycin

63
Q

MOA of macrolides

A
  • reversibly binds to the P site of the 50S ribosomal unit and inhibits RNA dependent protein synthesis by stimulating the dissociation of the peptide-tRNA from ribosomes
  • typically bacteriostatic
64
Q

What macrolide is inactivated by acid?

A

Erythromycin, therefore needs to be in a enteric coating

65
Q

What are macrolide active against?

A
  1. gram positive and gram negative
  2. anaerobes
  3. bacteria that are resistance to beta lactam
66
Q

What are macrolides resistant against?

A
  • resistance is due to reduced permeability of the cell membrane or active efflux, modification of the ribosomal binding site by chromosomal mutation, and/or production of esterase that hydrolyzes the macrolides
  • resistant to pneumococci
67
Q

macrolides precaution and contraindications

A
  1. prolonged QTc and torsades therefore should use with caution in patients on antiarrhythmic drugs, patients with uncorrected electrolytes, or any type of heart conditions
  2. avoid in patients with MS
  3. caution in patients with renal and hepatic impairment
  4. no specific caution in older adults
  5. safe for pregos and breastfeeding
  6. safe for pediatrics
68
Q

ADR in macrolides

A
  1. most common are GI symptoms and taste disturbances
  2. cdiff
  3. liver abnormalities
  4. Steven johnson syndrome, urticaria, eczema
  5. rare incidents of irreversible hearing loss
  6. hyperkinesia, dizziness and agitation in children
  7. dry mouth and dysphagia and stomatitis
69
Q

drug interactions in macrolides are

A
  1. has the most drug interactions due to strong inhibitors of CYP enzymes
  2. dig and warfarin - effects with be increased
  3. pimozide (for Tourettes) - causes serious dysrhythmias
  4. use caution in drugs that also prolongs QTc
  5. antacids slows absorption of macrolides
70
Q

clinical use for macrolides are

A
  1. community acquired PNA
  2. STIs
  3. H pylori
  4. MAC - mycobacterium avian complex in AIDS patients
  5. acne
  6. patients are who allergic to PNC and needs endocarditis prophylaxis
  7. Lyme disease
  8. pre op prep of the bowel
  9. gastroperesis
  10. ophthalmia neonatorum and chlamydia conjunctivitis and chlamydia neonatorum in newborns
71
Q

What is fidaxomicin?

A

a macrolide but has different MOA, spectrum of activity, pharmacokinetics, and uses

72
Q

MOA of fidaxomicin?

A

binds to RNA and inhibits RNA synthesis, a bactericidal

73
Q

What is fidaxomicin active against?

A

primarily c.diff

74
Q

What is fidaxomicin resistant against?

A

its rare and is not related to resistance with other macrocodes or other antibiotic classes

75
Q

fidaxomicin precaution and contraindication

A
  1. macrolide allergies
  2. safe for prego but not much research
  3. not sure if excreted in breast milk
  4. dosing does not need to be adjusted in hepatic impairment
  5. safety has not been evaluated for patients 18 and younger
76
Q

ADR of fidaxomicin are

A
  1. acute dyspnea, angioedema, rash/pruritus
  2. GI symtoms but more likely from cdiff
77
Q

Drug interactions with fidaxomicin are

A
  1. synergist effects with rifampin or rifaximin
78
Q

What drugs are in the oxazolidinones?

A
  1. Linezolid and Tedizolid
79
Q

MOA of oxazolidinones are

A

inhibitors of bacterial ribosomal protein synthesis, but unlike other antibiotics, they stop the first step in synthesis in which bacteria assemble ribosomes from their dissociated subunits by binding to 50S subunit and preventing 70S formation

cross resistance is unlikely

80
Q

What are oxazolidinones active against

A
  1. aerobic gram positive
  2. the most resistant forms of enterococcus including VRE and staph aureus
  3. mycobacterium tuberculosis
81
Q

What are oxazolidinones resistant against

A
  1. Enterococci and S aureus
82
Q

Oxazolidinones precaution and contraindications

A
  1. use or use within two weeks of a MAOI in contraindicated because can cause serotonin syndrome or increased BP
  2. Myelosuppression, CBC should ne monitored
  3. Lactic acidosis can occur, monitor acidosis
  4. long term use has been associated with peripheral neuropathy and optic neuropathy
  5. use for prego only if really needed risk v benefit
  6. is excreted in breast milk, use with caution
  7. can be used in infants and children
83
Q

ADR in oxazolidinones

A
  1. diarrhea, headache, and nausea
  2. cdiff
  3. myelosuppression
84
Q

Drug interactions with oxazolidinones are

A
  1. Linezolid is a reversible, non selective inhibitor MAOI
  2. interactions with MAOI when using with indirect action sympathomimetics, vasopressors, or dopaminergic drugs
  3. can also interact with SSRIs
  4. watch for serotonin syndrome
  5. interacts with tyramine rich foods and beverages
85
Q

Clinical use of oxazolidinones are

A
  1. MRSA PNA, use as an alternative to Vanco
  2. uncomplicated skin and skin structure infections MRSA/VRE, but not first line defense
  3. VRE faecium infections but can only be used for 28 days
86
Q

rational drug selection for Linezolid

A
  1. good for MRSA and VRE but not used as first line due to cost, drug interactions, and adverse effects with long term use
  2. high oral bioavailability if the IV alternative is too expensive
  3. should be reserved for mod to severe infections and only if the alternative is not beneficial
87
Q

MOA of sulfonamides

A
  1. has bacteriostatic actions
  2. competitively inhibits dihydrofolate synthetase, this prevents folic acid synthesis which is required for bacteria to make nucleic acids and purines
  3. usually not given by itself and is combined with trimethoprim
88
Q

sulfanomides are active against

A
  1. gram negative and gram positive
89
Q

sulfonamides are resistant against

A
  1. streptococci skin infections and chronic and recurrent UTIs
  2. resistance is due to mutations that causes excessive production of PABA therefore bacteria can make folic acid
90
Q

MOA of trimethoprim

A
  1. inhibits bacterial dihydrofolic acid reductase, preventing synthesis of purines which then converts to DNA
  2. usually used with sulfamethoxazole
91
Q

trimethoprim is active against

A
  1. gram negative and gram positive
  2. not active against enterococci because it uses extrinsic folic acid
92
Q

trimethoprim is resistant against

A
  1. resistance is due to reduced cell permeability, overproduction of dihydrofolate reductase or production of an altered reductase with less drug binding ability
93
Q

MOA of nitrofurantoin

A
  1. inhibits protein synthesis, aerobic energy metabolism, DNA and RNA synthesis, and cell wall synthesis but altering or inactivating bacterial ribosomes and other macromolecules
94
Q

nitrofurantoin is active against

A
  1. gram positive cocci and gram negative bacilli that causes UTIs
95
Q

nitrofurantoin is resistant against

A
  1. resistance is rare but there can be some plasmid mediated resistance transferable to susceptible organisms
96
Q

MOA of fosfomycin

A
  1. bactericidal antibiotic, available only in oral forms for UTIs
  2. inactivates the enzyme enolpyruvyl transverse which leads to inhibition of cell synthesis
  3. reduces bacterial adherence to epithelial cells in the urinary tract
97
Q

what is fosfomycin active against?

A
  1. most UTI pathogens plus pseudomonas
98
Q

what is fosfomycin resistant against?

A
  1. uncommon but is caused by enzymatic modifications of fosfomycin
99
Q

sulfonamides, trimethoprim, and nitrofurantoin precautions and contraindications

A
  1. patients with G6PD deficiency, renal impairment, and folate deficiencies
  2. nitrofurantoin and fosfomycin are not indicated for the treatment of pyelonephritis or perinephric abscess
  3. sulfa should not be used in prego, trimethprime use alone in prego should be used cautiously, the combination should not be used at all, nitrofurantoin and fosfomycin is safe for prego
  4. sulfa, nitro is okay for breastfeeding, trimethoprim should be used cautiously, and fosfomycin is not sure so don’t do it
  5. sulfa should not be used in children under 2 months and should be avoided in patients <6 years, trimethprim not sure yet about using under 2 months, nitro is contraindicated under 1 month, fosfomycin not sure about patients under 12 years
100
Q

ADR in sulfa, trime, nitro, and fosfo are

A
  1. GI symtoms
  2. C.diff
  3. sulfa/trime - rashes and gen skin eruptions and Steven Johnson syndrome
  4. sulfa and nitro - hepatic impairment
  5. sulfa - photosensitivity - use PABA free sunscreen
  6. trime - hyperkalemia
  7. nitro - peripheral neuropathy
  8. trime/sulfa - CNS adverse effects and aseptic meningitis
  9. nitro - pulm, toxicity
101
Q

Drug interactions in sulfa, trime, nitro, and fosfo are

A
  1. sulfa - warfarin, salicylates, and hydantoins
  2. sulfa/trime - increased cardiac QTc, watch out for other antiarrythmics and Qtc prolonged drugs
102
Q

Clinical use for trime, sulfa, fosfo, and nitro are

A
  1. UTIs
  2. trime/sulfa - community MRSA
  3. no longer used for sinusitis or otitis media
  4. PNA in patients with HIV
103
Q

rational drug selection for trime, sulfa, nitro, fosfo

A
  1. sulfa/trime - useful low cost agents for UTIs when proven susceptible, affordable and effective for MRSA infections compared to IV Vanco or oral linezolid unless infection is severe then use IV Vanco
  2. nitro and fosfo - empirical treatment of cystitis but nitro is cheaper if patient has no renal impairment
104
Q

MOA of tetracyclines

A
  1. inhibits protein synthesis by reverisbly binding to to the 30S subunit of the bacterial ribosome an preventing the addition of amino acids to growing peptides
  2. also have anti-inflammatory mechanisms that are useful for acne
105
Q

tetracyclines are active against

A
  1. gram positive and negative organisms and intracellular organisms
106
Q

tetracyclines are resistant caused by

A
  1. decreased intracellular accumulation due to impaired influx or increased efflux of an active transport protein pump
  2. ribosomal protection by proteins that interfere with drug binding
  3. enzymatic inactivation
107
Q

tetracyclines precaution and contraindication

A
  1. renal and hepatic impairment
  2. not for prego
  3. can be for breastfeeding patients
  4. should not be used for patients younger than 8 years
108
Q

ADR of tetracyclines are

A
  1. GI symtoms
  2. esophageal ulcers
  3. lightheadedness, dizziness, and vertigo
  4. photosensitivity and Steven Johnson syndrome
109
Q

Drug interactions with tetracyclines are

A
  1. antacids, iron salts, sevelamer, mag products, and zinc causes decreased antibiotic therapy
  2. increased warfarin effects
  3. may or may not affect oral contraceptives
110
Q

clinical use for tetracyclines are

A
  1. STIs
  2. acne
  3. H pylori
  4. doxy - primary choice for ehrichiosis and rickettsial infections, prophylaxis malaria and intestinal amebiasis
  5. minocycline - primary choice for mycobacterium marine
111
Q

rational drug selection for tetracyclines are

A
  1. doxy and mino require fewer daily doses than other tetracyclines and can be taken with meals
  2. doxy can be used for children if it is the treatment of choice for the disease, otherwise would be discouraged
112
Q

MOA of glycopeptides

A
  1. inhibits cell wall synthesis by binding firmly to D-A1a-A-A1a terminus of nascent peptidoglycan pentapeptide and causes cell wall damage
113
Q

glycopeptides are active against

A
  1. Vanco - gram positive
114
Q

glycopeptides are resistant against

A
  1. enterococcus faecium and S aureus
  2. due to modification of the binding site of the peptidoglycan building block
115
Q

glycopeptides contraindication and precautions

A
  1. oral vanco should not be used for systemic infections due to poor absorption
  2. nephrotoxic
  3. monitor for vanco infusion syndrome
  4. oral vance is safe for prego but IV should weigh risk vs benefits
  5. can be use with breastfeeding with oral vanco
  6. can be used in children for serious infections
116
Q

ADR of glycopeptides are

A
  1. nephrotoxicity
  2. hematological effects
  3. skin rashes
  4. Vance infusion syndrome and skin rashes if admin too quickly
117
Q

drug interactions of glycopeptides are

A
  1. avoid using with other drugs that causes nephrotoxicity
118
Q

clinical use for glycopeptides

A
  1. oral vanco - cdiff
  2. staph enterocolitis
  3. not effective in any other intestinal infections esp if it is a gram negative
119
Q

MOA of antimycobacterials

A
  1. interferes with lipid and nucleic acid biosynthesis in growing organisms
  2. also inhibits synthesis of mycotic acids which is important constituent for mycobacteria cell walls and are not found in mammalian cells
120
Q

precaution and contraindications for antimycobacterials

A
  1. hepatoxicity
  2. peripheral neuropathy in HIV and prego
  3. renal impairment
  4. cautious in patients with DM
  5. hematological alterations can occur
  6. can cause visual disturbances so be careful in patients who are unable to report the visual changes
  7. only isoniazid is safe for prego, others should do risk v benefits except streptomycin (shouldn’t be used at all)
  8. safe for breastfeeding
  9. can be used in children except for streptomycin
121
Q

ADR in antimycobacterials are

A
  1. hypersensitivity reactions
  2. peripheral neuropathy
  3. elevated AST/ALTs
  4. GI symtoms
  5. ototoxicity
122
Q

drug interactions in antimycobacterials

A
  1. rifamycins are potent inducers of the CYP enzyme system and speed the metabolism of many drugs resulting in therapeutic failure
  2. can reduce effectiveness of the live bacillus calmette guerin vaccine
123
Q

clinical use for antimycobacterials

124
Q

rational drug selection for antimycobacterials are

NURS 572 (3 decks)

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