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PULM > drugs for bacterial pulmonary infections > Flashcards

drugs for bacterial pulmonary infections Flashcards

1
Q

describe the 4 major categories of penicillins

A
  1. natural penicillins
  2. anti-staphylococcal (penicillinase-resistant) penicillins
  3. Amino penicillins (Extended spectrum)
  4. Anti-pseudomonal
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2
Q

MOA of penicillins

A

beta-lactams that bind to and inhibit transpeptidation of the peptidoglycan in bacterial cell walls (bacteriocidal)

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3
Q

what is augmentin?

A

amoxicillin + clavulanic acid

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4
Q

what does augmentin treat?

A

beta-lactamase producing staph aureus and other anaerobes producing respiratory tract infections

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5
Q

what is unasyn?

A

ampicillin + sulbactam

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6
Q

how is unasyn administered

A

parenteral

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7
Q

what is unasyn used for?

A

amp-resistant H. influenzae
moraxella catarrhalis
mixed G+ and anaerobic infections (CAP)

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8
Q

how do Clavulanic acid, Sulbactam and Tazobactam work?

A

they are suicide inhibitors that irreversibly acetylate the beta-lactamase enzyme

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9
Q

when should Penicillin V be given?

A

1 hour before or 2 hours after meal

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10
Q

how does food affect the absorption of penicillins?

A

generally decreases absorption (except amoxicillin)

gastric juices and decreased pH destroys PCN

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11
Q

how are penicillins metabolized?

A

hepatic enzymes (increased in pts w/ renal impairment)

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12
Q

how are the penicillins excreted?

A

renal tubular secretion (90%)

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13
Q

what 2 important things can affect the half life of penicillin?

A
  1. physiological state of the kidneys

2. concomitant therapy w/ drugs that are organic acids (drugs compete w/ penicillin for excretion by the kidneys)

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14
Q

if you have a pt w/ renal dysfunction how might you change the way you prescribe penicillins?

A

increase the dosing interval

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15
Q

what are 5 important adverse effects of penicillins?

A
  1. N/V (frequent w/ children)
  2. diarrhea after oral dose (killed gut flora)
  3. abnormal plasma electrolytes (in hypokalemic pt)
  4. renal impairment-dose related (Penicillin G)
  5. neurotoxicity w/ large doses (likely in pts w/ reduced renal function)
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16
Q

How long do delayed allergic rxns to penicillins take?

A

2 days (rashes)

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17
Q

how long do accelerated pencillin allergic reactions take?

A

30 mins to 48 hrs (hives, wheezing ,mild laryngeal edema, local inflamm. rxns)

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18
Q

what are the symptoms associated with penicillin acute allergic reaction?

A

anaphylaxis

bronchospasm

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19
Q

How do cephalosporins work?

A

bind to PBPs on bacterial cell membranes and inhibit bacterial cell wall synthesis similar to penicillins

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20
Q

Modifications at position 7(R1) of the beta-lactam ring are associated with_________________

A

alteration in antibacterial activity

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21
Q

Substitutions at position 3(R2) of the dihydrothiazine ring are associated with changes in ______________________

A

the metabolism and pharmacokinetic profile of the drug

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22
Q

what were the 3 reasons that cephalosporins were developed?

A
  1. be effective in pt allergic to penicillins
  2. to be effective against bacteria that are resistant to penicillins
  3. to have a broader spectrum
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23
Q

progression from 1st to 3rd generation cephalosporins are marked by what 4 things?

A
  1. broadening in gram negative susceptibility
  2. diminished activity against G+ bacteria
  3. increased resistance to beta-lactamase inactivation
  4. increased capability to enter the CSF
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24
Q

what are the 3rd generation cephalosporins used for?

A

enteric gram-negative organisms
reserved for very serious infections (crosses the BBB)
-H. influenza, Serratia, Pseudomonas (ceftazadime only)

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25
Q

whats unique about the 3rd generation cephalosporins?

A

penetrate the CSF enough to treat meningitis

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26
Q

how are the cephalosporins excreted?

A

renal tubular mechanims

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27
Q

what happens to the serum levels of cephalosporins when taken with probenecid?

A

increased

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28
Q

what are the adverse reactions to cephalosporins?

A 
hypersensitivity
diarrhea & GI distrubance
severe pain w/ IM injections
Phlebitis from intravenous administration
nephrotoxicity at high dosage
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29
Q

which cephalosporin most commonly causes diarrhea and GI disturbance?

A

ceftriaxone

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30
Q

how do carbapenems work

A

chemically different than penicillins but still have beta-lactam ring structure (binds to transpeptidase and blocks the cross linking of the cell wall peptidoglycan strands)

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31
Q

what is one big advantage of the carbapenems over the penicillins?

A

carbapenems have high resistance to bacterial beta-lactamase (potent suicide inactivators)

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32
Q

which drug has the broadest spectrum of any beta-lactam antibiotic?

A

imipenem

33
Q

imipenem is administered with what drug?

A

cilastatin

34
Q

how does cilastatin work?

A

inhibitor of dehydropeptidase (in brush border of proximal renal tubule)
prevents breakdown of imipenem and renal toxicity
fixed combination–>primaxin

35
Q

how is imipenem administered?

A

IV w/ good distribution to body tissues, but not CSF

36
Q

how is imipenem excreted?

A

both glomerular filtration and active secretion

37
Q

how does probenecid affect the half life of imipenem?

A

IT DOESNT

38
Q

Which carbapenem is contraindicated in pts w/ CNS seizures?

A

imipenem

39
Q

what is the typical indication for imipenem-cilastatin combo?

A

serious infections of aerobic gram-negative bacilli, anaerobes, and staph aureus

40
Q

how do aminoglycosides work?

A

protein synthesis inhibitor by binding to 30S subunit:

  1. block formation of initiation complex
  2. cause misreading of the code on mRNA template
  3. inhibit translocation
41
Q

what’s so great about the aminoglycosides?

A

broad spectrum of activity

valuable in treating nosocomial infections

42
Q

how do the macrolides work?

A

binds reversibly to 50s ribosomal subunit and inhibits protein synthesis (bacteriostatic)

43
Q

Name the 3 macrolides?

A

erythromycin
azithromycin
clarithromycin

44
Q

which macrolide do you have to make sure that you are reaching the minimal inhibitory concentration?

A

erythromycin

45
Q

which macrolide diffuses into prostatic fluid and macrophages and is primarily excreted in bile and feces?

A

erythromycin

46
Q

What are the drugs of choice in legionnaire’s disease?

A

erythromycin, azithromycin

47
Q

what is the most frequent side effect of erythromycin?

A

GI upset

48
Q

what is an important drug interaction involved with erythromycin?

A

inhibits cytochrome P450 3A (possible QT elongation in combo w/ other CYP3A inhibitors)

49
Q

which drug causes cholestatic hepatitis and transient deafness?

A

erythromycin hypersensitivity reaction to estolate form (also contraindicated in pts with liver dysfunction b/c it accumulates in liver)

50
Q

Name this drug: more acid stable than erythromycin, absorption increases w/ food, undergoes rapid first pass metabolism with active primary metabolite, eliminated by kidney and liver.

A

clarithromycin

51
Q

Name this macrolide: t 1/2 40-68 hours

A

azithromycin

52
Q

how is the majority of azithromycin excreted?

A

in bile

53
Q

which macrolide has a major advantage over the others in that it doesn’t inhibit any CYP enzymes?

A

azithromycin

54
Q

how do the quinolones work?

A

inhibits DNA replication via binding to DNA gyrase and topoisomerase IV (bactericidal)

55
Q

What are 2 ways that resistance is developing to fluroquinolones by less drug getting to the target enzyme?

A
  1. decrease number of porin proteins in the outer membrane (impairing access to intracellular gyrase) 2. decreased intracellular accumulation of drug via efflux pumps
56
Q

what can bind to and negatively affect the absorption of oral fluoroquinolones?

A

divalent, trivalent cations (iron, zinc supplements)

57
Q

what are the important side effects of fluoroquinolones?

A

photosensitivity
prolongation of QT interval (moxifloxacin)
articular cartilage erosion
GI upsets

58
Q

how do the tetracyclines work?

A

inhibit protein synthesis by reversible binding to 30S ribosome (bacteriostatic, MIC must be maintained)

59
Q

how can resistance to tetracyclines develop?

A
  1. increased efflux of tetracycline from cell
  2. decreased transport
    (resistance to one tetracycline provides resistance to all )
60
Q

what are the main indications for tetracyclines?

A

atypical pneumonias, dental disease

61
Q

what can inhibit the absorption of tetracyclines?

A

di, trivalent cations

62
Q

how are most tetracyclines removed from the blood?

A

removed by liver, also undergoes enterohepatic cycling

63
Q

how are tetracyclines distributed?

A
  • wide tissue distribution and cross the placental barrier

- bone and teeth when undergoing calcification (discolors teeth)

64
Q

what are some adverse effects of tetracyclines?

A
  1. GI disturbance (N/V/D, avitaminosis, superinfections)
  2. chelation of Ca2+ (discoloration of teeth)
  3. depression of bone growth
  4. hepatic toxicity
  5. photosensitivity (doxycycline)
65
Q

which tetracycline is less likely to cause superinfections?

A

doxycycline

66
Q

what are the advantages to using doxycycline over other tetracyclines?

A
  1. requires fewer doses (100% bioavailability)
  2. less GI disturbance
  3. available oral and parenteral
  4. no dosage adjustment required for reduced renal function
67
Q

what are the therapeutic uses of tetracyclines?

A 
atypical pneumonia (doxycycline)
Lyme disease
Rickettsial infections
periodontal disease
acne
68
Q

what is first line therapy for nocardiosis?

A

TMP/SMX

69
Q

none of the cephalosporins work against which bug?

A

enterococcus

70
Q

what are the adverse effects of imipenem?

A

SEIZURES (beware w/ renal insufficiency)
CNS toxicity
allergic reactions
expensive!

71
Q

how can resistance to erythromycin develop?

A

plasmid mediated processes

  • decreased transport
  • modification of target by methylases
  • hydrolysis of drug from hydrolases
72
Q

name of the phenotype that has a gene that encodes methylases that modify the macrolide binding to the ribosome and confers resitance to all 3 macrolides?

A

MLSb from the erm gene via a plasma mediated process

73
Q

how is erythromycin excreted?

A

in bile and feces

74
Q

what are the important drug interactions for clarithromycin?

A

also CYP3A4 inhibit but not as much as erythromycin

75
Q

which macrolide has impaired absorption with food?

A

azithromycin

76
Q

how is resistance developing against fluorquinolones regarding DNA gyrase binding?

A

Mutation in QRDR of DNA gyrase enzyme

77
Q

which tetracycline can be given to pts w/ renal dysfunction without adjustment of dose?

A

doxycycline

78
Q

what patients don’t get tetracyclines?

A

pregnant women and kids under 9 yrs

79
Q

what do the fluoroquinolones treat?

A

Pneumococcus (levofloxacin, moxifloxacin)
Staph Aureus
bunch of gram negatives

PULM (14 decks)

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