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NUR370 > Antibiotics > Flashcards

Antibiotics Flashcards

1
Q

Gram Staining Test

A
  • Examines bacteria under microscope after applying a stain
  • “Gram positive” have a thick cell wall and retain the stain
    “Gram negative” have a thin cell wall and do not retain the stain
  • Important pathogenic and biochemical differences between gram positive and negative bacteria and their sensitivity to antibiotics
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2
Q

Shape of Bacteria

A
  • Examining bacteria under the microscope to determine shape
  • Rod shaped – called “bacillus/bacilli”
  • Spherical shaped – called “coccus/cocci”
  • Spiral shaped – called “spirilla”
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3
Q

Bacterial Respiration

A
  • “Aerobes” – thrive in oxygen-rich environment
  • “Anaerobes” – grow best without oxygen
  • Help us predict what bacteria would be involved in an infection (e.g. bowel vs skin infection)
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4
Q

Drugs that disrupt bacteria cell wall

A
  • Penicillins/cephalosporins/ carbapenems (beta-lactams)
  • Vancomycin
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5
Q

Drugs that disrupt bacterial biochemical reaction

A
  • Sulfonamides

- Trimethoprim

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6
Q

Drugs that disrupt bacterial DNA structure or synthesis

A
  • Fluoroquinolones

- Metronidazole

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7
Q

Drugs that inhibit bacteria protein synthesis

A
  • Macrolides
  • Aminoglycosides
  • Clindamycin
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8
Q

Bactericidal

A
  • Kill organism by cell lysis
  • Rely less on host immunity for clearing infection
  • Preferred for infection at sites of poor penetration
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9
Q

Bacteriostatic

A
  • Inhibit bacterial replication
  • Do not kill the organism but allow host immune system to clear infection
  • Good for people who have normal healthy immune system, because you rely on the host’s immune system to take care of the infection
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10
Q

“Match the bug to the drug”

A
  • Gram staining: cell wall structure, bacterial shape (relatively rapid, a couple hours)
  • Speciation: different tests to identify species (morphologic characteristics, biochemical tests, susceptibility tests, serologic tests, PCR or nucleic acid amplification tests
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11
Q

Culture and Sensitivity Test

A
  • sample is cultured in presence of antibiotics and growth is measured
  • information on sensitivity to different antibiotics
  • either sensitive (S), intermediate (I) or resistant (R)
  • Limitations: several days, don’t always culture, may not be causative, must be done before starting Abx, contamination
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12
Q

Empiric Antibiotic Selection

A
  • may have to start therapy before C&S results come back
  • choose an Abx based on knowledge of bacteria usually causing infection at that site
  • Normal flora: bacteria normally reading in a given area, protect against invasion by pathogenic bacteria (can cause infection)
  • Skin, nasopharynx, pharynx: Staphylococcus, Streptococcus
  • Stomach: Helicobacter Pylori
  • Bowel: Bacteroides, E. coli, enterococcus
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13
Q

Factors affecting normal flora

A
  • Disease states (e.g. COPD, smokers)
  • Where patient lives/works
    - Hospitalized patients (and health
    care workers) have  proportion of
    gram negatives
  • Previous/recent antibiotic use
    • May allow overgrowth of resistant
      bacteria
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14
Q

Host Defenses

A
  • Antibiotics work together with patient’s immune system to resolve infection (goal of therapy is to suppress growth to the point at which balance is tipped in favour of host)
  • Immunosuppressed patients (e.g. patients receiving cancer chemotherapy, transplant patients, AIDS, etc.) may need more aggressive treatment
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15
Q

Site of Infection

A

Antibiotics must get to site of infection to work
Generally have poor penetration to:
- Brain (i.e. meningitis)
- Bone (i.e. osteomyelitis)
- Heart (i.e. endocarditis)
- Abscesses – require surgical drainage
Need increased doses to sites of poor penetration

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16
Q

Considerations during Pregnancy

A
  • Some agents cross placenta and may impact fetal development – need to choose wisely
  • Generally considered safe in pregnancy: Pencillins, cephalosporins, clindamycin, erythromycin (most forms), azithromycin
  • Avoid in pregnancy: Fluoroquinolones, Septra, tetracyclines, metronidazole
  • Others - weigh risk vs. benefit, may depend on trimester
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17
Q

Age

A
  • Agents due to poor drug metabolism or elimination
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18
Q

Allergies

A
  • 1-10% of patients
  • Range from mild (e.g. maculopapular rash) to severe (anaphylaxis)
  • Drugs with similar structure (e.g. penicillins and cephalosporins) may be cross-reactive although this has been overestimated in the past
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19
Q

Combination Therapy

A
  • Additive response: antimicrobial effect = sum of effects of each agent
  • Synergistic response: antimicrobial effect > sum of effects of each agent
  • Antagonistic response: when combining a bactericidal agent with bacteriostatic agent
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20
Q

When to Use Combination Therapy

A

Combinations may be appropriate for:

  1. Initial therapy of severe infection (esp. in immunocompromised patients)
  2. Mixed infections with multiple infecting organisms (e.g. brain abscess, pelvic infection)
  3. Prevention of resistance (e.g. tuberculosis)
  4. Decreasing toxicity (allows for  doses)
  5. Synergistic activity (esp. for hard to kill bugs such as Pseudomonas)
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21
Q

Antibiotic Dosing

A

Patient weight (some drugs dosed mg/kg)
Site of infection
Route of elimination: change to dosing regimen needed for renally eliminated agents in patients with renal impairment
Time vs. concentration-dependent killing

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22
Q

Minimum Inhibitory Concentration (MIC)

A
  • Lowest concentration of antibiotic required to inhibit visible bacterial growth in vitro
  • Correlates to dosage regimen or amount of Abx required for clinical efficacy
  • Need serum and tissue concentrations to exceed the MIC to be effective
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23
Q

Time-Dependent Killing

A
  • Rate and extent of killing determined by length of time drug level remains above MIC
  • e.g. penicillins, cephalosporins, erythromycin
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24
Q

Concentration-Dependent Killing

A
  • Rate and extent of killing improved with high peak drug concentration
  • e.g. aminoglycosides, fluoroquinolones
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25
Q

Renal Dose Adjustment

A
  • Required for agents with high renal elimination
  • Time-dependent killing – better to decrease dose
    • Beta-lactams,
      cephalosporins
      (most),
      sulfonamides
  • Concentration-dependent killing – better to increase interval
    • Fluoroquinolones,
      aminoglycosides,
      vancomycin
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26
Q

When to Start Therapy?

A

START: Clinical suspicion of infection (signs and symptoms)–> Start ASAP (Higher rates of cure and lower mortality when therapy started early)

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27
Q

When to Stop Therapy?

A
  • Do not stop prematurely (risk of recurrent infection that is more treatment resistant)
  • Do not use for too long (risk of resistance)
  • Duration variable according to host factors, organism, site of infection; 7 to 14 days is a common duration
  • Host defences (immunocompromised), site of infection, pathogen, repeat cultures are negative, pt response
28
Q

Patient Assessment and Monitoring

A
  • Fever (less pronounced in elderly, debilitated, immunocompromised)
    • chills, rigors, may
      see decreased
      temperature in
      severe infection
  • Affect
  • Leukocytosis (increased WBC and neutrophils)
  • Metabolism - catabolic response (loss of nitrogen, Mg, K, PO4-)
  • CV effects (increased HR, RR, decreased BP)
  • Renal effects: Proteinuria, dehydration and decreased BP/renal perfusion/urine output
  • Site-specific symptoms (UTI vs pneumonia vs meningitis)
29
Q

Efficacy Evaluation

A 
- For most infections, signs and symptoms should start to improve within 1 day
When to be concerned:
     - Fever 
       unresolved after 
       3 days
     - Increasing signs 
       and symptoms
     - Continued 
       symptoms after 
       course of 
       therapy 
       complete
- Need to re-evaluate patient and antibiotic selection
30
Q

Prophylaxis

A
  • Use when suspected or anticipated exposure to pathogenic organism (e.g. travel, contact with known infected person, surgery, etc.)
  • Use minimum duration possible
  • Surgical procedures, bacterial endocarditis, neutropenia, other (recurrent UTI, HIV+, immunosuppressed)
31
Q

Bacterial Resistance

A
  • Growing problem
  • Drugs which were once effective are now useless against resistant organisms
  • Examples of resistant bugs (“superbugs”): VRE, MRSA, E. coli, Pseudomonas aeruginosa
  • Leading cause is misuse
  • Bacteria adapt structure/function (increase drug metabolizing enzyme, decrease active uptake of drugs, change microbial drug receptors, synthesize compounds that antagonize drug action)
  • Bigger problem with broad spectrum
    Contributing factors
  • Failure to follow infection control practices
  • Omission of surgical drainage (e.g. abscesses), catheter removal
  • Medication error
  • Medication non-adherence
  • Self-medicating or antibiotic sharing
32
Q

Examples of Antibiotic Misuse

A
  • Wrong drug:
    use of broad spectrum agent to treat highly susceptible bacteria/incorrect drug selection for pathogen
  • Wrong dose (esp. sub-therapeutic)
  • Wrong timing (esp. starting too late)
  • Wrong duration
  • Use in viral infection (e.g. common cold)
  • Treatment of fever of unknown origin in immunocompetent patient
33
Q

Promoting Appropriate Antibiotic Use

A
  • Specificity
  • Appropriate duration/route
  • Surgical prophylaxis: within 30 min of first cut, usually continue no more than 24 hrs post-op
  • Timing
  • Right dose, TDM
  • Outpatient therapy
34
Q

Natural Penicillins

A
  • Penicillin G = IV form (not orally bioavailable)
  • Penicillin V = oral form (stable in stomach acid)
  • Common therapeutic uses (Infections caused by sensitive gram positive cocci (e.g. Streptococcus)
  • -> some pneumonia, endocarditis, meningitis cases
  • Narrow spectrum, inactivated by penicillinases (Most staphylococci produce penicillinases making them resistant to natural penicillins)
35
Q

Bacterial Resistance to Penicillin

A
  • Bacteria produce enzyme (“beta-lactamase” aka “penicillinase”) that cleaves the β-lactam ring to inactivate penicillin
36
Q

Penicillinase-Resistant Penicillins

A
  • Prototype: cloxacillin
  • Resist inactivation by penicillinase (only agents in penicillin class that are effective against staphylococcus)
  • Common therapeutic uses (uncomplicated skin and soft tissue infection)
  • Not effective against MRSA = Methicillin Resistant Staph Aureus (bacterial strain with altered PBPs to which penicillins cannot bind)
37
Q

Aminopenicillins

A
  • Main agents: ampicillin (IV/PO), amoxicillin (PO)
  • Broader spectrum active against some gram negative bugs (e.g. E. Coli) due to ability to penetrate gram negative cell envelope
  • Common therapeutic uses: UTI, respiratory tract infection, otitis media
  • Amoxicillin preferred over ampicillin for oral use (higher bioavailability, less diarrhea)
38
Q

Antipseudomonal Penicillins

A
  • Main agent: piperacillin (IV)
  • Even broader spectrum due to even better ability to penetrate gram negative cell envelope (Active against Pseudomonas)
  • Common therapeutic uses: serious infections (e.g. sepsis) due to Pseudomonas, especially in the immunocompromised host…often combined with other anti-pseudomonal agents (e.g. aminoglycosides)
39
Q

Penicillins + Beta-Lactamase Inhibitor

A
  • Combining penicillin with a beta-lactamase inhibitor broadens spectrum of activity. Common examples:
    Amoxicillin + clavulinic acid (Clavulin®) (PO),
    Piperacillin + tazobactam (Tazocin®) (IV)
  • Only available in fixed-dose combinations
40
Q

Cephalosporins

A
  • All names start with “ceph-” or “cef-”
  • Most widely used class of agents, very safe
  • 4 ‘generations’ available in Canada
  • As increase generation:
    more resistant to beta-lactamases, increase gram negative, decrease gram positive coverage, increase CSF penetration
41
Q

Cephalosporins (Examples and Uses)

A

First generation (cefazolin IV, cephalexin PO)
- Skin and soft tissue infections
- Surgical site infection prophylaxis
Second generation (cefaclor PO, cefuroxime PO/IV)
- Respiratory tract infections
Third (e.g. ceftriaxone, ceftazidime) and fourth generation (e.g. cefepime IV)
- Empiric therapy in severe infections (meningitis, febrile neutropenia)

42
Q

Carbapenems

A
  • Names end in “-penem”
  • Broadest spectrum agents available
  • Generally resistant to pencillinases
  • Reserve for infections not susceptible to narrower spectrum agents
  • Parenteral forms only
  • e.g. imipenem, meropenem
43
Q

Beta-Lactams: Side Effects

A
  • GI: nausea, vomiting, diarrhea
  • Neurologic: seizures (penicillins; imipenem at high IV doses – avoid if seizure history)
  • Dermatologic: thrombophlebitis (minimize by diluting solution and slowing infusion time)
  • Allergic reactions (0.4-7% with penicillins)
    -range from mild
    (rash) to severe
    (anaphylaxis)
    • generally avoid
      penicillins unless
      benefits outweigh
      risks
    • avoid
      cephalosporins/
      carbapenems
      only if
      reaction to
      penicillin is severe
      (estimated 1%
      cross reactivity)
44
Q

Antibiotic Allergy

A
  • Symptoms: itching, rash, swelling (face, tongue, lips), urticaria, flushing, dizziness, syncope, wheezing, throat tightness, trouble breathing
  • Most occur early (monitor with first dose) but delayed reactions possible
  • Educate patient on symptoms
  • Patients with known antibiotic allergy should carry wallet card or wear Medic Alert bracelet
  • Management: antihistamines, corticosteroids, epinephrine
45
Q

Beta-Lactams: Pharmacokinetics and Drug Interactions

A
  • Most have short half-lives, dosed 3 to 4 times daily (some exceptions)
  • Some have better absorption if taken on empty stomach (e.g. cloxacillin)
  • Most require renal dose adjustment
  • Combo of aminoglycosides + beta-lactams can increase bacterial killing
    • But… must not
      be mixed
      together in IV
      bag due to
      direct chemical
      interaction
46
Q

Vancomycin

A
  • Mechanism of action: inhibits cell wall synthesis (bactericidal)
  • Large molecule, not orally absorbed
  • Common therapeutic uses: Drug of choice for MRSA, treatment of serious infections in penicillin-allergic patients, C. difficile (only if given orally)
  • IV and PO forms: oral used for gut infections such as C. Difficile
  • Renal dose adjustment required (IV only): therapeutic drug monitoring used to titrate dosing regimen –> “trough” level drawn immediately before dose is due
47
Q

Vancomycin: Side Effects

A

Dermatologic: “Red Man Syndrome”
- Histamine-mediated reaction – flushing of trunk, neck and face; hypotension
-Prevention/ management:
slow infusion rate (i.e. extend infusion time from 1 hour to 2 hours), pre-medicate with antihistamine
- Not a true allergic reaction, does not preclude future use
Renal: nephrotoxicity (~5%)
- Minimize risk with therapeutic drug monitoring in at risk patients (avoid high trough levels)

48
Q

Aminoglycosides

A
  • Prototype: tobramycin
  • Mechanism of action: disrupt bacterial protein synthesis (bactericidal)
  • Large, positively charged molecules, not orally absorbed
  • Common therapeutic uses: serious gram negative infections (e.g. Pseudomonas) or gram positive infections (if combine with beta-lactam), ophthalmic/otic infections
49
Q

Aminoglycosides: Drug Interactions

A
  • Combo of aminoglycosides + beta-lactams or vancomycin can increase bacterial killing. But… must not be mixed together in IV bag due to direct chemical interaction
  • Increased risk of renal damage if combined with other nephrotoxic drugs (e.g. vancomycin, NSAIDs)
50
Q

Aminoglycosides: Side Effects

A

Renal: nephrotoxicity (usually reversible)
- monitor serum creatinine, avoid in renal impairment where possible
Neurologic
- Ototoxicity – tinnitus (ringing in ears), vertigo, headache; may be irreversible
- Paresthesias, seizures
- Monitor and advise patient to report symptoms
Increased risk if high trough levels and prolonged duration
- Therapeutic drug monitoring and once daily dosing help to reduce risk

51
Q

Aminoglycosides: Dosing and Administration

A
  • Once daily dosing preferred over traditional dosing (3 times daily)
    • Higher peak = more effective (recall: concentration- dependent killing)
    • Post-antibiotic effect = washout period = safer
    • More convenient
      Renal dose adjustment required
      Therapeutic drug monitoring used to titrate dosing regimen  “trough” levels
      Formulations: parenteral, eye/ear drops
52
Q

Macrolides

A
  • Erythro-, clarithro- and azithromycin
  • Inhibit bacterial protein synthesis (bacteriostatic)
  • Common therapeutic uses: respiratory tract infections (e.g. pneumonia), chlamydia, diphtheria, alternative to penicillin in allergic patients
53
Q

Macrolides: Side Effects and Drug Interactions

A

GI: nausea/vomiting, diarrhea
- occurs with PO and IV formulations
- worst with erythro-
Erythro- and clarithro-
- inhibit CYP450 enzymes – increase levels of theophylline, CBZ, warfarin
Azithro – do not take with Al3+/Mg2+/Ca2+ containing products
Macrolides antagonize effects of clindamycin (bind to the same target)

54
Q

Macrolides: Dosing and Administration

A
  • PO and IV formulations
  • Erythromycin – dosed TID to QID (various prodcts, food may decrease absorption)
  • Clarithromycin – dosed once or twice daily
  • Azithromycin – dosed once daily( Long half-life, loading dose commonly used –> double dose on first day, Shorter treatment duration (“Z-Pak” = 5 days))
55
Q

Fluoroquinolones

A
  • Prototype: ciprofloxacin
  • Names end in “-floxacin”
  • Mechanism of action: inhibit bacterial DNA synthesis and replication (bactericidal)
  • Common therapeutic uses: UTI, pneumonia, infection of bones, joints, skin, soft tissue and gut infection (e.g. traveller’s diarrhea), ophthalmic/otic infections
56
Q

Fluoroquinolones: Side Effects

A
  • GI: nausea, vomiting, diarrhea
  • Neurologic: headache, dizziness, peripheral neuropathy
  • MSK: joint/muscle pain, tendinitis, tendon rupture, cartilage growth suppression – avoid in pregnancy and age < 13
57
Q

Fluoroquinolones: Drug Interactions, Dosing and Administration

A
  • Decreased -bioavailability if taken together with dairy products, antacids (Ca2+/Mg2+), minerals (Ca2+, iron) – space apart by ≥ 2 hours
  • IV, PO, eye and ear preparations
  • Once or twice daily
  • Renal dose adjustment required
58
Q

Sulfonamides

A
  • Main agent in use today is sulfamethoxazole + trimethoprim (Septra®)
  • Mechanism of action: disrupt folate synthesis so bacteria cannot make DNA, RNA, protein (bacteriostatic)
  • Common therapeutic uses: UTI, Pneumocystis carinii pneumonia (PCP) – now known as Pneumocystis jiroveci
59
Q

Sulfonamides: Side Effects

A
  • Hypersensitivity reactions (~3%): mild rash, drug fever, photosensitivity are most common, Stevens-Johnson syndrome rare but high mortality, Key patient education points – stop taking if rash occurs, minimize sun exposure
    Hematologic: decreases WBC/ platelets, hemolytic anemia (rare)
  • GI: nausea, vomiting, diarrhea
60
Q

Sulfonamides: Drug Interactions

A
  • Highly protein bound – will displace other protein bound drugs (Warfarin, phenytoin, sulfonylureas_
  • “Sulfa” allergy and cross-reactivity: very little data to support cross-reactivity between sulfonamide antibiotics and other “sulfa” drugs (e.g. HCTZ, furosemide, sulfonylureas); often combined and generally considered safe
61
Q

Sulfonamides: Dosing and Administration

A
  • Sulfamethoxazole – used in fixed dose combination with trimethoprim (Septra®); PO and IV forms
  • Dosing usually once or twice daily
  • IV form may be given up to 4 times daily in treatment of severe infections
  • Renal dose adjustment required
62
Q

Clindamycin

A
  • Mechanism of action: inhibits bacterial protein synthesis (bacteriostatic)
  • Common therapeutic uses: mixed infections with gram positive and anaerobes (skin and soft tissue, aspiration pneumonia), abdominal and pelvic infections, alternative to penicillins in beta-lactam allergy
63
Q

Clindamycin: Side Effects, Dosing and Administration

A

GI: DIARRHEA
- May indicate infection with C. difficile
- High vigilance needed – stop clindamycin if significant diarrhea
Key patient education point: report significant diarrhea to MD (≥ 5 watery stools per day)
Oral dose QID, IV dosed TID

64
Q

Clostridium Difficile (“C. Diff”)

A
  • Aka antibiotic-associated diarrhea, pseudo- membranous colitis
  • C. difficile (anaerobic gram positive bacilli) spores ingested –> overgrowth in gut when competing gut flora wiped out by recent antibiotic use
  • Profuse watery diarrhea, abdo pain, fever, increased WBC
  • Can occur during or after Abx therapy (PO and IV) –> Clindamycin, fluoroquinolones, 3rd generation cephs
  • High morbidity and mortality
  • Must monitor and report diarrhea
65
Q

C. Difficile Treatment and Prevention

A

Treatment
- PO metronidazole or PO vancomycin
- Discontinue any precipitating antibiotics
- Avoid anti-diarrheal agents which decrease bowel motility (e.g. loperamide (Imodium®), opioids)
Prevention
- Proper antibiotic prescribing
- Infection control practices (i.e. contact isolation, strict hand hygiene, Chlorox cleanser to kill spores)
- ↑ risk with acid suppressing drugs (e.g. proton pump inhibitors) – minimize use where possible

66
Q

Metronidazole (Flagyl®)

A
  • Mechanism of action: disrupt DNA synthesis (bactericidal)
  • Common therapeutic uses: drug of choice for C. difficile, treatment of anaerobic infections of CNS, abdomen, bone, joint, skin, soft tissue, pelvis, prophylaxis of surgical site infection (abdominal, colorectal, gyne surgery), treatment of protozoal infections (not discussed)
  • PO and IV forms
  • Dosed 2 to 3 times daily
67
Q

Metronidazole: Side Effects and Drug Interactions

A
  • GI: nausea, vomiting, diarrhea, metallic taste
  • Neurologic: dizziness, vertigo
  • Other: brown urine discoloration (harmless)
  • Alcohol – serious contraindication: inhibits aldehyde dehydrogenase, leads to build up of alcohol metabolite acetaldehyde –> headache, n/v, flushing, SOB , must warn patients to avoid alcohol during treatment and for 3 days after

NUR370 (2 decks)

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