💊370: Antibiotics Flashcards

1
Q

What are the shape classifications of bacteria?

A
  1. Bacillus/bacilli - Rod shaped
  2. Coccus/cocci - Spherical
  3. Spirilla - Spiral
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2
Q

Bactericidal

A

Kill organism by cell lysis

For infection at sites of poor penetration

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3
Q

Bacteriostatic

A

Inhibit bacterial replication

Rely on host immune system (thus not immunocompromised)

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4
Q

Speciation

A

Identify bacterial species

Biochemical tests, PCR, etc

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5
Q

Culture and Sensitivity (C&S) Testing

A

Sensitive (S)
Intermediate (I)
Resistant (R)

To each antibiotic tested

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6
Q

Which sites do antibiotics generally have poor penetration to?

A
  1. Brain
  2. Bone
  3. Heart
  4. Abscesses - require surgical drainage

Need ⬆️ doses to sites of poor penetration

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7
Q

Which antibiotics should be avoided in pregnancy as they cross the placenta?

A
  1. Fluoroquinones
  2. Metronidazole
  3. Septra (Trimethoprim)
  4. Tetracyclines

(For Mother’s Safe-T Treatment)

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8
Q

What are the different effects of combination therapy?

A
  1. Additive response
  2. Synergistic response
  3. Antagonistic response
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9
Q

When is antibiotic combination therapy used?

A
  1. Severe infection
  2. Multiple infections
  3. Resistance prevention
  4. Decreasing toxicity (dec doses)
  5. Synergistic activity
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10
Q

What are factors to consider during antibiotic dosing?

A
  1. Weight
  2. Site of infection
  3. Route of elimination
  4. Time- vs concentration-dependent killing
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11
Q

What is the Minimum Inhibitory Concentration (MIC)?

A

Lowest concentration of antibiotic required to inhibit visible bacterial growth in vitro

Lower MIC = more effective antibiotic against that organism

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12
Q

Time-dependent killing Antibiotics

A

Determined length of time drug remains above MIC

Ex. Penicillins, cephalosporins, erythromycin

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13
Q

Concentration-dependent killing Antibiotics

A

Rate and extent of killing improved with high peak drug concentration

Ex. Aminoglycosides, fluoroquinolones

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14
Q

Renal Dose Adjustment

A

Required for agents with high renal elimination

Time-dependent killing = ⬇️ dose

Concentration-dependent killing = ⬆️ interval

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15
Q

What factors help determine when to stop antibiotic treatment?

A
  1. Host defenses
  2. Site of infection
  3. Infecting pathogen
  4. Negative cultures
  5. Patient response
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16
Q

Patient assessment and monitoring on antibiotic treatments?

A
  1. Leukocytes (⬆️WBC, ⬆️neutrophils)
  2. Metabolism (⬇️ nitrogen, Mg2+, K+, PO4-)
  3. CV effects (⬆️HR, ⬆️RR, ⬇️BP)
  4. Renal effects (Proteinuria, dehydration, ⬇️ renal perfusion, ⬇️urine output)
  5. Site-specific symptoms (UTI, pneumonia, meningitis)
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17
Q

When should a nurse be concerned while evaluating antibiotic efficacy?

A
  1. Fever unresolved after 3 days
  2. Signs and symptoms increased/unresolved
  3. Continued symptoms after course of therapy complete
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18
Q

What are common indications for antibiotic prophylaxis?

A
  1. Surgical procedures
  2. Bacterial endocarditis
  3. Neutropenia
  4. Other (recurrent UTI, HIV+, transplant, immunosuppression)
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19
Q

What are examples of resistant strains (“superbugs”)?

A
  1. Enterococcus (VRE)
  2. Staphylococcus aureus (MRSA)
  3. Escherichia coli
  4. Pseudomonas aeruginosa
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20
Q

What is the leading cause of antibiotic resistance?

A

Misuse and overuse of antibiotics

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21
Q

How do bacteria become resistant?

A

Adaptive changes:

  1. Drug metabolizing enzymes
  2. Decreased uptake of drugs
  3. Microbial drug receptors
  4. Synthesis of compounds that antagonize drug action
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22
Q

What is the mechanism of action of Beta-Lactam Antibiotics?

A

Inhibit bacterial cell wall synthesis
(Bactericidal)

Target penicillin-binding protein (PBP) on cell cytoplasmic membrane (basis of selectivity)

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23
Q

What are drug classes of Beta-Lactam antibiotics?

A
  1. Penicillins
  2. Cephalosporins
  3. Carbapenems
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24
Q

What are types of penicillins?

A
  1. Natural penicillins (narrow spectrum)
  2. Penicillinase-resistant penicillins
  3. Aminopenicillins
  4. Extended-spectrum penicillins
  5. Penicillins + beta-lactamase inhibitor
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25
Q

Why does penicillin resistance arise?

A

Penicillinase

Gram negative cell envelope

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26
Q

What are natural penicillins?

A

Penicillin G = IV form
Penicillin V = oral form

Narrow spectrum
Sensitive gram positive cocci

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27
Q

What is the mechanism of action of bacteria resistance to penicillin?

A

Bacteria produce enzyme beta-lactamase (penicillinase) that cleaves the Beta-lactam ring to inactivate penicillin

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28
Q

What is a prototype of penicillinase-resistant penicillins?

A

Cloxacillin

Only agent effective against staphylococcus
Not effective against MRSA

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29
Q

What are the main agents of aminopenicillins?

A

Ampicillin (IV/PO)
Amoxicillin (PO)

Broader spectrum
Penetrate gram negative cell envelope

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30
Q

What are common therapeutic uses for aminopenicillins?

A

UTI
Respiratory tract infection
Otitis media

31
Q

What is the main agent of antipseudomonal penicillins?

A

Piperacillin (IV)

Broad spectrum (penetrated gram negative cell envelope)

Active against pseudomonas

32
Q

What are common therapeutic uses for antipseudomonal penicillins?

A

Serious infections (ie sepsis) due to Pseudomonas

33
Q

What is the use for penicillins + Beta-Lactamase inhibitors?

A

Broadens spectrum of activity

Amoxicillin + clauvinic Acid (Clavulin) (PO)
Piperacillin + tazobactam (Tazocin)(IV)

34
Q

Cephalosporins

A
  1. More resistant to beta-lactamases
  2. ⬆️ gram negative, ⬇️ gram positive
  3. ⬆️ CSF penetration

4 generations in Canada

35
Q

What are examples and common therapeutic uses of First generation cephalosporins?

A

Cefazolin IV, cephalexin PO

  1. Skin and soft tissue infections
  2. Surgical site infection prophylaxis
36
Q

What are examples and common therapeutic uses of Second generation cephalosporins?

A

Cefaclor PO, cefuroxime PO/IV

Respiratory tract infections

37
Q

What are examples and common therapeutic uses of Third and Fourth generation cephalosporins?

A

3rd: ceftriaxone, ceftazidime
4th: cefepime IV

Severe infections (meningitis, febrile neutropenia)

**3rd gen can lead to C-diff

38
Q

What are examples and therapeutic uses of Carbapenems?

A

Ex. Imipenem, meropenem

Broadest spectrum agents
Resistant to penicillinases

Parenteral forms ONLY

39
Q

What are side effects of Beta-Lactams?

A

GI: n/v, diarrhea

Neuro: seizures (penicillins; impenem at high IV doses)

Dermatologic: thrombophlebitis (minimize by diluting dilution and slowing infusión time)

Allergic reactions

40
Q

Antibiotic allergy

A

Symptoms: itching, rash, face swelling, urticaria, flushing, dizziness, syncope, wheezing, throat tightness, trouble breathing

Management: antihistamines, corticosteroids, epinephrine

41
Q

What are the pharmakinetics and drug interactions of Beta-Lactams?

A

Short half-lives

Better absorption on empty stomach (ex. Cloxacillin)

42
Q

What is the mechanism of action of Vancomycin?

A

Inhibits cell wall synthesis (bactericidal)

Large molecule, not orally absorbed

43
Q

What are common therapeutic uses for Vancomycin?

A
  1. MRSA
  2. Serious infections in penicillin-allergic pts
  3. C. difficile (only orally)
44
Q

Which antibiotic induces Red Man Syndrome?

A

Vancomycin

45
Q

What is Red Man Syndrome?

A

Histamine-mediated reaction

  • flushing of trunk, neck and face
  • hypotension

Management: slow infusion rate, antihistamines

46
Q

What are side effects of Vancomycin?

A
  1. Red Man Syndrome

2. Nephrotoxicity (avoid high trough levels)

47
Q

What are dosing and administration requirements of Vancomycin?

A

IV and PO forms

Renal dose adjustment required (IV only)

48
Q

What is a prototype of aminoglycosides?

A

Tobramycin

49
Q

What is the mechanism of action of aminoglycosides?

A

Disrupt bacterial protein synthesis (bactericidal)

Large, positively charged molecules

Not orally absorbed

50
Q

What are common therapeutic uses of aminoglycosides?

A
  1. Serious gram negative infections (ex. Pseudomonas)
  2. Gram positive infections (combined with bets-lactam)
  3. Ophthalmic/optic infections (eye or ear drops)
51
Q

What are drug interactions with aminoglycosides?

A
  1. Aminoglycosides + beata-lactams or Vancomycin can increase effectiveness BUT can’t be mixed in IV bag d/t chemical rxn
  2. Nephrotoxic drugs increase renal damage (ex. Vancomycin, NSAIDs)
52
Q

What are side effects of aminoglycosides?

A
  1. Nephrotoxicity (unreversible)
  2. Ototoxicity (tinnitus, headache, vertigo)
  3. Parasthesias, seizures

Increased risk if high trough levels and prolonged duration

53
Q

What is the dosing and administration of aminoglycosides?

A

Higher peak = more effective (concentration-dependent killing)

Post-antibiotic effect = washout period = safer

Renal dose adjustment required

PARENTAL, eye/ear drops

54
Q

What are types of macrolides?

A

Erythro-
Clarithro-
Azithromycin

55
Q

What is the mechanism of action for macrolides?

A

Inhibit bacterial protein synthesis (bacteriostatic)

56
Q

What are common therapeutic uses for macrolides?

A
  1. Respiratory tract infections (ex. Pneumonia)
  2. Chlamydia, diphtheria
  3. Alternative to penicillin-allergic pts
57
Q

What are side effects of Macrolides?

A
  1. GI: n/v, diarrhea
  2. Erythro- and clarithro- inhibit CYP450 enzymes
  3. Azithro- do not take with Aluminum, Mg2+, Ca2+
  4. Antagonize effects of clindamycin
58
Q

What are therapeutic uses for Flourquinolones?

A
  1. UTIs
  2. Pneumonia
  3. Infection of bones/joints/soft tissue
  4. Gut infection (travellers diarrhea)
  5. Opth/optic infections
59
Q

What are specific drug interactions with Flourquinolones?

A

Bioavailability decreases with Dairy, antacids, minerals (Ca/Mg/Iron)

60
Q

What are side effects of Flourquinolones?

A
  1. N/v, diarrhea
  2. Headache, dizziness
  3. Peripheral neuropathy
  4. MSK pain
  5. Tendinitis, tendon rupture
  6. Cartilage growth suppression

**could lead to c.diff

61
Q

What is a prototype of Flourquinolones?

A

Ciprofloxin

“-floxin”

(IV, PO, ear/eye drops)

62
Q

What is a prototype of Metronidazoles?

A

Flagyl

PO, IV

63
Q

What are common therapeutic uses for Metronidazoles?

A
  1. C. difficile
  2. Anaerobic infections of CNS/abdomen/bone/joint/soft tissue/pelvis
  3. Surgical prophylaxis
  4. Protazoal infections (the tail- Flagyl!)
64
Q

What are common side effects of Metronidazoles?

A
  1. N/v, diarrhea
  2. Metallic taste
  3. Dizziness, vertigo
  4. Brown urine
65
Q

What are specific drug interactions with Metronidazoles?

A

ALCOHOL

Inhibits aldehyde dehydrogenase, leads to build up of acetaldehyde

  • headache, n/v, flushing, SOB
66
Q

What is the mechanism of action for Sulfonamides?

A

Disrupt folate synthesis do bacteria cannot make DNA/RNA/proteins

67
Q

What are 2 prototypes of Sulfonamides?

A
  1. Sulfamethoxazole
  2. Trimethoprim (Septra)

(PO, IV)

68
Q

What are therapeutic uses for Sulfonamides?

A
  1. UTIs

2. PCP (pneumocystis carnii pneumonia, AKA Pneumoncystis jiroveci)

69
Q

What are specific drug interactions with Sulfonamides?

A

Highly protein bound - displace other drugs
(Warfarin, phenytoin, Sulfonylureas)

**Sulfa allergy

70
Q

What are side effects of Sulfonamides?

A
  1. Hypertensitivity rxn (mild rash fever, photosensitivity)
  2. Low WBC/platelets
  3. Hemolytic anemia (rare)
  4. N/v, diarrhea
  5. STEVENS-JOHNSON Syndrome
71
Q

What is the mechanism of action for Clindamycins?

A

Inhibit bacterial protein synthesis

BACTERIOSTATIC

72
Q

What are therapeutic uses for Clindamycins?

A
  1. Mixed infections
  2. Skin/soft tissue
  3. Aspiration pneumonia
  4. Abdominal/pelvic infections
  5. Alternative to penicillin
73
Q

What are common side effects of Clindamycins?

A

DIARRHEA (lead to C.diff)