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Pharmacology > Intro to antibiotics > Flashcards

Intro to antibiotics Flashcards

1
Q

Bactericidal

A
  • drugs that are directly lethal to bacteria at clinically achievable concentrations.
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2
Q

What populations are bactericidal drugs used in?

A

immunocompromised pts, (HIV, chemo, organ transplant) -> immune system suppressed/ decreased by other meds

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3
Q

Bactericidal drugs

A 
-Penicillin, Cephalosporins, Carbapenems, Vancomycin 
(cell wall inhibitors) 
-Aminoglycosides  
-TMP/SMX 
-Fluoroquinolones  
-Metronidazole
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4
Q

Bacteriostatic drugs

A

CMT-S

  • Clindamycin
  • Macrolides
  • Tetracycline
  • Sulfanimides used alone
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5
Q

Bacteriostatic

A
  • drugs that slow down bacterial growth but do not cause cell death
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6
Q

Bacteriostatic drugs are used in what patients

A
  • Healthy patients -» immune system takes over and finishes the job by the use of phagocytes
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7
Q

Prototype

A
  • a drug that best represents an antibiotic category; doesn’t mean they are the most ordered or prescribed, just has the best characteristics that describe them.
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8
Q

Prophylaxis

A

→ preventing infection, pre-surgery, special populations (heart valves, rheumatic fever, dental surgeries)

  • If antibiotics are used post-surgery → indicates an infection is being treated
  • Immunosuppressed patients (Ex: give Bactrim to an HIV patient to prevent PJP)
  • Systemic antibiotic prophylaxis: IV antibiotics; given broad-spectrum antibiotics two hours before surgery.
  • Used with major operations (bowel surgery, C-section, joint replacement) NOT minor surgeries
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9
Q

Empiric therapy

A

-using our best guess to what organism is causing the infection
Ex: most common cause of UTIs is E. coli → use an antibiotic to treat E. coli (gram-negative rod)
Drug selection based on clinical evaluation and knowledge of which microbes are most likely to cause infection at a particular site; used as an initial treatment in patients with severe infections.

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10
Q

aerobic microbes

A

grow in the presence of oxygen

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11
Q

anaerobic microbes

A

-can grow in the absence of oxygen; harder to treat!
Locations: deep wounds, tissues, and internal organs
Infections: abscess formation, tissue destruction, foul-smelling pus
- Can be gram - or gram +
- C.Diff, e. Coli, clostridium botulinim, clostridium tetani

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12
Q

Abx used for anaerobic microbes

A

Treatment: Flagyl (metronidazole), Clindamycin

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13
Q

Narrow spectrum ABX

A

active against only a few species of microbes.
-antibiotics active against GP-cocci and GP-bacill → PCN G, Vancomycin, Erythromycin, Clindamycin

-Ex: antibiotics active against GN-aerobes → Aminoglycosides, Cephalosporins (1st & 2nd Gens)

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14
Q

Broad Spectrum ABX

A
  • Active against a wide variety of microbes
  • Antibiotic active against both GP cocci and GN-bacilli → Cephalosporins (3rd & 5th Gens), Tetracycline, Carbapenems (imipenem), TMP/SMX, Fluoroquinolones (Ciprofloxacin)
    ○ Can markedly alter normal flora
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15
Q

1st step to choosing an ABX

A

1) The identity of the infecting organism
○ Gram stain (and plating): quickest & simplest technique to identify microbes
■ performed to identify Gram-positive vs. Gram-negative, Shape (bacilli, cocci, spirilla), and metabolism requirements (aerobic versus anaerobic)
■ Gram-positive bacteria: Staph, Strep, Enterococcus
■ Gram-negative bacteria: E. coli, Shigella, Salmonella, Klebsiella, Enterobacter, Serratia marcescens, Proteus mirabilis/vulgaris, Haemophilus, Neisseria, Pseudomonas, clostridium

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16
Q

What are cultures, when are they taken, how long do they take?

A
  • used to identify the pathogen
    ■ Taken BEFORE anti-infectives are started!!
    ■ Can take 2-5 days (Knowlton said 48 hours)
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17
Q

2nd step to choosing an ABX

A

2) Drug sensitivity of the infecting organism
○ Once bacterial growth occurs, it’s performed to identify which antibiotics are effective in killing the bacteria.
○ Uses Minimum Inhibitory Concentration (MIC): susceptibility to an antibiotic (not complete death).
○ NOT ALWAYS NEEDED; used more with pathogens with known resistance (staph)

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18
Q

3rd Step to choosing an ABX

A

3) Host factors (site of infection, status of host defenses–healthy vs immunocompromised)
-● PCR testing is also used for pathogen identification
○ Ex: MRSA, HIV, CGAMD

19
Q

Selective toxicity

A
  • antibiotics that are harmful to the microbe but NOT the human host.
    -○ Achieved by using antibiotics that work by manipulating the biochemical processes of the microbe and not the host.
    ■ Disruption of bacterial cell wall
    ■ Inhibition of an enzyme unique to bacteria
    ■ Disruption of protein synthesis
20
Q

Initial tx for severe infections needing immediate tx

A

Broad-spectrum

21
Q

Need to obtain specimens for identification ……..

A
  • before treatment

- ■ Antibiotics can suppress microbial growth in culture and confound identification

22
Q

After C&S and identification of the pathogen what abx do you use?

A

Narrow-spectrum (more selective antibiotic)

23
Q

Factors that determine abx therapy

A
  • Allergy, ability to penetrate, immunocompromised patinet, age, genetics, Foreign hardware in body
24
Q

Medication allergy

A

○ Most common causes of allergic reactions: Penicillins, cephalosporins, sulfa-drugs, and erythromycin

25
Q

intolerance

A

Nausea and vomiting

26
Q

Allergic reaction

A

itching, skin rashes, hives, SOB

27
Q

Anaphylactic rxn

A

can develop within 1 hr of taking the dose, and include difficulty breathing, shortness of breath, Respiratory stridor, and angioedema, severe hypotension, tachycardia, bronchospasm

28
Q

If patient suspects anaphylaxis symptoms..

A

discontinue medication and notify provider

29
Q

Ability to penetrate the site

A

○ Meningitis: drug needs to be able to cross BBB
■ Cephalosporins (Gen 3-5)
○ Abscess: tend to be caused by anaerobes; need to flush it out first for treatment to be effective
■ Metronidazole (Flagyl), vancomycin

30
Q

immunocompromised pt/ host

A

Use bactericidal antibiotics

31
Q

Foreign hardware within the body

A
  • Need to use Bactericidal versus bacteriostatic antibiotics because phagocytes may try to “eat” the hardware.
  • Makes phagocytes less able to attack bacteria if they’re attacking hardware, thereby allowing microbes to flourish
  • Treatment often results in failure or relapse and may require removal of the hardware
32
Q

Age: infants

A

high risk for toxicity →
■ FROM EXAM 1:
■ organ system immaturity; drug responses are unusually intense and prolonged
■ Elevated drug levels= more intense response
■ Delayed elimination= prolonged response
■ Metabolism- Markedly faster until age 2, then gradual decline → Increase dose or increase intervals
■ <2 yrs. → smaller dose due to greater rate of metabolism, delayed elimination
■ >2 yrs.→ gradual ↑; larger or more frequent dose due to gradual decline of metabolism, & increasing elimination
■ Topical absorption much greater in kids → Possible Permethrin Question?
■ BBB not formed until 1 year

33
Q

Age: Children/ adolescents

A

: avoid use of certain drugs (Tetracyclines)

34
Q

Age: pregancy and lactation

A

risk to mom AND fetus (Gentamicin causes hearing loss; Sulfonamides cause kernicterus in nursing newborns)

35
Q

Age: older adults

A

heightened drug sensitivity
■ FROM EXAM 1:
■ Absorption → delayed gastric emptying
■ Distribution → Increased body fat (drug storage); Decreased muscle mass (less protein-binding sites)
■ Metabolism → Decreased activity of hepatic enzymes → decreased hepatic metabolism
■ Excretion → Decline in renal function; GFR decreases

36
Q

Genetic Factors

A

○ Sulfonamides are contraindicated for patients with G6PD deficiency (causes anemia)
○ slow, rapid, normal metabolizers

37
Q

How does antibiotic Resistance work?

A

○ Host contains lots of microbes where a few are drug resistant
○ Antibiotics kill bacteria causing the illness, as well as good bacteria protecting the body from infection.
○ The drug-resistant bacteria are now allowed to grow and take over.
○ Some bacteria give their drug-resistance to other bacteria, causing more problems

38
Q

Factors contributing to antibiotic resistance?

A

○ Spontaneous mutation
■ Change in DNA: Single drug resistance
■ Conjugation of chromosomal DNA: multi-drug resistance
■ HA-acquired infections are generally more resistant than community-acquired infections
○ Use of antibiotics in food supplies
○ Misuse (viral infections)
○ Overuse (bacteria mutate)

39
Q

Prevention methods for antibiotic resistance?

A

○ Antibiotic stewardship: giving antibiotics appropriately, and using them for the right amount of time.
○ Only take antibiotics when needed
■ NOT for viral infections (URI, otitis media)
■ Understand effect on microbe
○ Take full course of antibiotic
○ Take cultures before administering antibiotics
○ Discuss probiotics
○ Isolation precautions

40
Q

MDROs

A

○ MRSA, VRE, ESBL (Extended-spectrum Beta-lactamase producers

41
Q

Superinfections

A

● Superinfections: killing of host normal flora allows remaining microbes to grow and cause a new infection to occur.
-Ex: Yeast infection, Candidiasis in the mouth, C. diff
Be aware of possible superinfection with C. diff → Clindamycin* (most common), Fluroquinolones, cephalosporins, penicillins, vancomycin

42
Q

Gi Distress

A

N/V/D

43
Q

Allergic rxns

A

: rash, hives, difficulty breathing (SOB)
○ Assess BEFORE and AFTER administration
○ Dosage INDEPENDENT
○ Requires prior immune system priming → may occur during the second dose

44
Q

If allergic rxn occurs

A

■ STOP medication
■ Think about airway (ABCs); epinephrine
■ Call Rapid Response/Code Cart

Pharmacology (14 decks)

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