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CRRAB 2 Week 5 and 6 > Antibiotic Review > Flashcards

Antibiotic Review Flashcards

1
Q

What are the reasons for responsible prescription writing?

A

minimize the development of antibiotic resistant microorganisms

minimize harm to the patient caused by toxicity from unnecessary drugs

provide cost effective treatment

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2
Q

What are the Centor criteria and what do they tell you?

A

A centor score of 2 or higher, then there’s likely a bacterial infection so you should conduct a rapid antigen detection test

absence of cough = 1
age 3-14 = 1, 15-45 = 0, >45 = -1
anterior cervical LA = 1
fever = 1
tonsillar erythema or exudate = 1
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3
Q

What is a rapid strep test actually detecting?

A

C-carbohydrate on the bacteria’s outer membrane

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4
Q

What is the specificity and sensitivity of the rapid strep test? What does this mean in terms of diagnosis/

A

specificity is great - over 95%
sensitivity is relatively low at 80%

this means that you can get a lot of false negatives - need to follow any negative with sputum cultures

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5
Q

What’s the number one antibiotic of choice for strep pyogenes pharyngitis?

A

penicillin (and there really isn’t much resistance, so that’s good)

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6
Q

What are the 4 groups of beta-lactam meds?

A

penicillins
cephalosporins
carbapenems
aztreonam

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7
Q

What is the mechanism of action for the beta lactam ABx?

A

they bind to the penicillin binding protein, which is a transpeptidase required for the peptide-linking step in cell wall synthesis

you get a build-up of cell wall rpecursors, which activates autolytic enzymes

ultimately you get cell lysis = bactericidal

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8
Q

When would you consider using penicillin G over penicillin V? What’s the greater risk with G?

A

Use G if you’re concerned about compliance - you only have to give one injection in the office

the risk for anaphylaxis is higher with G than V

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9
Q

Amoxicillin is also used for treatment of strep pyogenes, but why is penicillin preferable?

A

it’s super broad spectrum so you need to worry about killing normal flora

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10
Q

What should you give in anaphylaxis? What is the effect on vasculature? On pulmonary system?

A

epinephrine - induces vasoconstriction via alpha1, tachycardia via beta1 and bronchodilation via beta2

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11
Q

What other drugs should you avoid if a person has a hypersensitivity to penicillin? What’s ok?

A

avoid cephalosporins and carbapenems = cross-sensitivity

aztreonam is okay because it’s a monobactam

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12
Q

Why wouldn’t aztreonam work for strep pharyngitis though?

A

it’s only effective against gram negatives

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13
Q

So what should you give a patient with a penicillin allergy if he has strep pharyngitis?

A

Have to go to a macrolide or clindamycin

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14
Q

What are the three macrolides we know?

A

erythromycin
azithromycin
clarithromycin

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15
Q

What is the mechanism of action for the macrolides?

A

bind to the 23s rRNA of the 50S subunit, inhibiting translocation

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16
Q

What’s the spectrum of macrolides?

A

broad coverage of respiratory pathogens

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17
Q

How do bacteria get resistance against macrolides? Two ways….

A

methylation of the 23s binding site

increased efflux

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18
Q

What are the adverse effects of macrolides?

A 
GI discomfort (stimulates migratory motor complex)
prolonged QT
hepatic failure (inhibits CYP3A4)
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19
Q

Which macrolide is counterindicated in pregnancy?

A

clarithromycin - associated with miscarriages

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20
Q

Treatment failure ocurs in 15% of positive GAS cases. What are potential reasons for this?

A
  1. antibiotic resistance - rare for penicillin, but 5-8% resistant to macrolides
  2. lack of compliance
  3. had a viral pharyngitis, but was a carrier for GAS
  4. neighboring flora like H. flu secrete beta-lactamases
  5. Strep pyogenes can enter epithelial cells and hide from ABx
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21
Q

Treatment for influenza is usually just supportive, but what groups of people do you treat?

A 
those with severe illness
over 65 yrs old
under 2 years old
pregnant
with chronic illnesses
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22
Q

What are the two groups of influenza antivirals?

A

adamantane (amantadine)

neuraminidases (oseltamivir and zanamivir)

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23
Q

What does adamantane block?

A

viral uncoating

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24
Q

Why is adamantane not really used anymore?

A

It was only effective against influenza A in the first place and now the vast majority of strains are resistant to it

(change in viral M2 proton ion channel)

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25
Q

What do oseltamivir and zanamivir do?

A

They block the effects of neuraminidase such that you don’t get the cleavage step necessary for viral spread

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26
Q

When are oseltamivir and zanamivir effective? In what strains?

A

when the virus is in the actively dividing phase - so treat within the first 48 hours of symptom onset

effective for influenza A and B but not C

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27
Q

Why can resistance develop so quickly for influenza?

A

high mutation rates - viral polymerase makes a lot of mistakes

leads to antigenic drift and shift

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28
Q

Describe oseltamivir a little more:

age for use, metabolism, excretion, side effects

A

use in people over 1 yr of age
prodrug needs to be activated by hepatic esterases
renal excretion (so modify for renal insufficiency)
GI side effects, HA and fatigue

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29
Q

Describe zanamivir in more detail:

age of use, how is it taken? why is this important?, who do you avoid it in?

A

Use in people over 7 years
you inhale it, but only 10-20% reaches the lung
the remainder in the oropharynx can cause bronchospsm, so avoid in patients with asthma and other pulmonary diseases

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30
Q

Why do we treat the high-risk flu cases? Is it because of flu complications?

A

it’s not necessarily the flu we’re worried about - it’s the secondary bacterial pneumonia that kills people

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31
Q

What is another term for secondary infection after a previous infections?

A

superinfection

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32
Q

Why does influenza promote secondary pneumronia?

A

causes apoptosis of airway epithelial cells so you have inhibition of mucocilliary clearance

also, the neuraminidase enhances bacterial growth

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33
Q

What are the organisms to think of for secondary pneumonia after influenza? According to Amy…

A

strep pneumoniae
staph aureus
GAS

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34
Q

CXR confirmation is often unnecessary for a diagnosis of community-acquired pneumoniae, so any antibiotic treatment you initiate without a CXR is considered what? What should you do before that though?

A

empiric

take a sputum sample for gram stain and culture first though

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35
Q

What are the common etiologies of community-acquired pneumonia?

A 
mycoplasma neumoniae
respiratory viruses
strep pneumoniae
chlamydia pneumoniae
legionella
hamemophilus influenzae
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36
Q

Do empiric and definitive ABx treatment really differ in terms of pneumoniae treatment?

A

no differences in mortality rates or length of hospitalization

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37
Q

What are examples of broad spectrum ABx?

A 
carbapenems
chloramphenicol
3rd gen fluoroqhinolones
2nd, 3rd and 4th gen caphalosporins
tetracyclines
38
Q

What are examples of narrow spectrum ABx?

A 
penicillin
lincosamides
glycopeptides
streptogramins
Rifamycin
39
Q

What are the two main antibiotic choices for comunity-acquired pneumoniae uncomplicated by other lung pathology?

A

doxycycline or a macrolide

40
Q

What ABx should you use for CAP in patients with comorbidities or ABx use within the past 3 months?

A

a respiratory fluoroquinolone

or a high-dose beta-lactam plus macrolide

41
Q

What are the 4 general mechanisms of drug resistance?

A
  1. Alteration in drug target
  2. enzymatic inactivation
  3. decreased uptake
  4. increased efflux
42
Q

For strep pneumoniae, what is the cause of the penicillin resistance?

A

mutation in penicillin binding protein (so can’t really use a beta lactam with a betalactamase)

43
Q

For strep pneumoniae, what is the cause of macrolide resistance? Two things…

A
  1. alteration of ribosomal binding site

2. increased efflux

44
Q

The pneumococcal vaccine was introduced in about 2000. What effect did the vaccine have on resistance to macrolides?

A

it wasn’t really effective against drug-resistant serotypes, so now 90% of strains are now resistant to macrolides

45
Q

What are the three respiratory fluoroquinolones?

A

gemifloxacin
levofloxacin
moxifloxacin

46
Q

What is the mechanism for the fluoroquinolones? Bactericidal or static?

A

they directly inhibit DNA replication by binding bacterial DNA topoisomerase II (gyrase - gram neg) and topo IV (gram pos)

bactericidal!

47
Q

What is the spectrum of coverage for the respiratory fluoroquinolones?

A

broad: gram positive, negative and atypicals like mycoplasma

48
Q

What are the two causes of resistance to fluoroquinolones?

A

active efflux

mutation of topoisomerase binding sites

49
Q

What are the side effects of the fluoroquinolones? Counterindicated in what groups?

A

GI discomfort
tenindopathies

Don’t use in pregnancy, lactation or children

50
Q

What two antibiotics are typically used for mycoplasma pneumoniae?

A

doxyxycline or azithromycin

can’t use a betalactam obviously bc it doesn’t have a cell wall

51
Q

Mycoplasma pneumoniae is hard to culture, so how do you make diagnosis?

A

test for cold agglutinins (IgM)

52
Q

What is the mechanism of action for the tetracyclines like doxycycline? Cidal or static?

A

They bind to the 30S subunit preventing attachment of aminoacyle tRNA, disrupting protein synthesis

bacteristatic

53
Q

Why is spectrum of tetracyclines so limited? What can you use it for?

A

Resistance is so widespread

use for B. burgdorferi (lyme disease), H. pylori and mycoplasma pneumoniae. Will NOT work against gram negative rods

54
Q

What are the two main mechanisms of resistance to tetracyclines?

A
  1. reduced uptake

2. increased efflux

55
Q

What are the adverse effects of tetracycline? Contraindicated in what groups?

A

photosensitivity, discoloration of teeth, inhibition of bone growth

avoid in pregnancy and children

don’t take with milk - oral absorption limited by cations

56
Q

Does doxycycline exhibit concentration-dependent killing or time-dependent killing? What does this mean for treatment strategy?

A

concentration-dependent

means you need to get the concentration over 10 times the minimum inhibitory concentration

57
Q

What group of ABx are especially time-dependent and how does this affect treatment strategy?

A

the beta lactams - this is why you need to have multiple doses for a longer course

58
Q

What are the three main nosocomal pneumonias?

A

MRSA
pseudomonas aeruginosa
klebsiella pneumoniae

59
Q

What are the two drugs you can give to treat MRSA pneumonia? Why not daptomycin?

A

give vancomycin or linezolid

can’t use daptomycin because it’s inactivated by pulmonary surfactant

60
Q

What ABx can you give for pseudomonas aeruginosa?

A

piperacillin/taxobactam with cefepime (4th gen ceph)

imipenem/cilastatin, aztreonam

61
Q

How do you treat klebsiella pneuoniae if it has carbapenemases?

A

extended spectrum beta-lactamase with colistin-polymixin E

62
Q

How does vancomycin work?

spectrum?

A

it’s a glycopeptide that inhibits cell wall synthesis by binding to the D-ala D-ala dipeptide , inhibiting the transglycosylation reaction

mainly effective against gram positives

63
Q

What is the mechanism of action for linezolid? Spectrum?

A

it’s an oxazolidone that targets the 50S ribosome and inhibits protein synthesis

mainly effective against gram-positive organisms like staph, enterococci, and strep

64
Q

Infections with gram negative bacilli are particularly common in what group?

A

CF patients

65
Q

What is the mechanism of polymyxin E/colistin? Spectrum?

A

it binds phosphatidylethanolamine in the membrane, creating holes

used for multidrug resistant gram negatives like klebsiella

66
Q

What’s the side effect of polymyxin E/colistin that makes it a drug of last resort?

A

nephrotoxicity

67
Q

How does resistance to polymyxin E develop?

A

trick question - resistance is super infrquent and slow to develop - no cross-resistance with any other ABx

68
Q

Describe the general pathogenesis of histoplasmosis? What kind of fungus is it?

A

It’s dimorphic:

In the environment it is a mold with hyphae and connidia. The connidia are released as spores, which we inhale into our lungs. In the lungs the spores bud into a yeast.

69
Q

What will you see microscopically in a histo infection?

A

reticuloendothelial cells

70
Q

Where is histo most common?

A

the mississippi/ohio river valleys

71
Q

What will blastomyces dermatitidis look like microscopically?

A

broad-based yeast

72
Q

Where is blastomyces endemic?

A

inhabits rotting wood in the eastern US

73
Q

What will coccidioides immitis look like microscopically?

A

endospores in a spherule

74
Q

Where is coccidioides endemic?

A

in the US southwest - needs dry climates

75
Q

Where can fungal pneumonias disseminate in immunosuppressed individuals?

A

bones, joints and CNS

76
Q

What is the mechanism of action for amphotericin B?

A

It’s a polyene that binds ergosterol to create holes in the fungal membrane allowing leakage of electrolytes

77
Q

What is the spectrum for amphotericin B?

A

used for invasive systemic fungal infections in immunocompromised patients - active against both yeasts and molds

78
Q

What are the adverse effects of amphotericin B and why does basically everyone have side effects?

A

it’s super toxic because it can bind to cholesterol (which is everywhere for us).

decreases renal blood flow and can lad to permanent destruction of the basement membrane - 80% will have nephrotoxicity

79
Q

How does resistance develop against amphotericin B?

A

It rarely happens, but you can have degreased ergosterol in the membrane

80
Q

What are the four general issues aspergillus fumigatus can cause?

A
  1. allergic bornchopulmonary aspergillosis - just a hypersensitivity reactions (reaction to brown mucous plugs containing fungi and eosinophils) - most common in asthma or CF
  2. aspergillomas - fungal balls in lungs
  3. fungal sinusitis
  4. systemic disease in immunocompromised
81
Q

If the aspergillus is systemic, how do you treat it?

A

with voriconazole

82
Q

Why is mortality rate between 45-80% with systemic disease even with voriconazole?

A

patients are often severely neutropenic due to immune compromise and just can’t clear the infection

83
Q

Why is prednisone sufficient for treating the alelrgic bronchopulmonary aspergillosis?

A

it’s just a hypersensitivity reaction - no fungus has actually invaded the body

84
Q

What is the mechanism of action of the axoles like voriconazole and itraconazole?

A

they bind the fungal p450 enzyme Erg11, thus blocking the production of ergosterol and causing the accumulation of a toxic intermediate called lanosterol

85
Q

What are the major toxicities of the azoles?

A

drug-drug interactions, hepatotoxicity, neurotoxicity, altered hormone synthesis (so avoid during pregnancy)

86
Q

What are the 2 main causes of resistance against the azoles?

A

altered Erg11

upregulation of efflux

87
Q

What agents can be used for symptomatic treatment of respiratory infections?

A
  1. antitussives to block cough refluex
  2. expectorants to thin mucus
  3. NSAIDs for analgesia and fever reduction
  4. decongestants - constrict blood vessels in nasal mucosa
  5. anti-histamines
  6. bronchodilators
  7. supplemental O2
  8. nebulized cold steam
  9. corticosteroids
88
Q

What are some home-substances that can be effective prophylaxis against respiratory infections?

A

garlic
vitamin C
Echinacea
probiotics

89
Q

What are some reasons by patients should be careful about consuming combination or products?

A
  1. decongestants and antiH1 = make mucus thicker
  2. might end up taking too much analgesics!
  3. may help symptoms, but the symptoms like cough may have been helping them clear the infection
  4. no better at relieving symptoms than blacebo (alcohol, benzocaine, expectorants, codeine, antihistamine monotherapy)
90
Q

Why shouldn’t you give cough medicines to kids under 4?

A

the risk of ovredose is too high and you don’t get much benefit

CRRAB 2 Week 5 and 6 (6 decks)

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