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Pharmacology - Fall > Lecture 15 - Antibiotics & Antituberculars > Flashcards

Lecture 15 - Antibiotics & Antituberculars Flashcards

1
Q

When are antibiotics needed for sinus infections?

A
  • Thick or green mucus doesn’t indicate a sinus infection

- Needed for some lasting over 7 days or severe infections

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2
Q

When are antibiotics needed for a sore throat?

A

Most often caused by viruses, but strep throat needs antibiotics

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3
Q

Do colds respond to antibiotics?

A

No b/c caused by viruses

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4
Q

What normally causes symptoms of upper respiratory tract infections?

A

Toxins released by pathogens and the inflammatory response to fight the infection

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5
Q

Majority of infections are caused by ____

A

Viruses

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6
Q

When should antibiotics be recommended for upper respiratory tract infections?

A

Confirmation of significant bacterial cultures in sputum

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7
Q

Which diseases pose a serious threat due to antibiotic resistance?

A
  • Carbopenem resistant enteritis
  • Vancomycin resistant enterococci
  • Tuberculosis
  • Staph aureus skin infections
  • C. difficile food poisoning
  • Gonorrhea
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8
Q

Which organism is resistant to almost all antibiotics?

A

Enterobacter

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9
Q

What is the current recommended treatment for gonorrhea?

A

Combination therapy of injectable cephalosporin and oral azithromycin

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10
Q

Which antibiotic is critically important for treating salmonella and E. coli infections?

A

Ampicillin

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11
Q

What are the causes of antibiotic resistance?

A
  • Overuse/abuse in humans
  • Overuse/abuse in non-humans
  • Developing countries
  • World travel
  • Critically ill px
  • Industry advertising/promoting
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12
Q

What increases the risk of antibiotic resistance infections?

A
  • Patient-related factors (increasing age and severity of underlying disease)
  • Hospital-related factors (increased length of stay, ICU, proximity to infected px)
  • Treatment-related factors (prolonged use of broad spectrum antibiotics, contaminated devices)
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13
Q

How do bacteria become antibiotic resistant?

A
  • Spontaneous mutation

- Acquisition of new DNA

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14
Q

How can bacteria acquire new DNA?

A
  • DNA comes from environment after being released by another cell
  • Virus transfers DNA btwn bacteria
  • Contact btwn cells as DNA crosses from donor to recipient
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15
Q

What are the possible mechanisms of acquired antibiotic resistance?

A
  • Alteration in target site

- Decreased uptake

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16
Q

What do beta-lactamases do?

A

Inactivate beta-lactam drugs through cleavage of their central ring structure (beta-lactam)

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17
Q

What is clavulanic acid?

A

Inhibitor of beta-lactamases

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18
Q

How can you overcome beta-lactamases?

A
  • Clavulanic acid
  • Combine penicillin w/ other antibiotic (ex: penicillin and clavulanic acid)
  • Add bulkier side chains to the basic penicillin structure, hindering enzyme access to the beta-lactam ring
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19
Q

What causes tetracycline resistance?

A

Decreased uptake or increased extrusion

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20
Q

What is the most common tetracycline resistance mechanism? What are some other mechanisms?

A
  • Mg2+-dependent active efflux mediated by the TetA gene
  • Other – bacterial enzymes that inactivate tetracyclines; expression of bacterial proteins that inhibit binding of tetracycline to ribosome
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21
Q

How can bacteria become resistant to aminoglycosides?

A
  • Decreased uptake of drug (absence of porin channels or oxygen-dependent transport system)
  • Enzymes inactivate aminoglycosides
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22
Q

Which enzyme inactivate aminoglycosides?

A
  • Acetyltransferases
  • Nucleotidyltransferases
  • Phosphotransferases
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23
Q

How can bacteria become resistant to macrolides?

A
  • Decreased uptake of drug
  • Increased efflux of drug
  • Reduced affinity for 50S ribosome
  • Enzyme inactivates macrolides (erythromycin esterase)
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24
Q

Is cross-resistance common for macrolides?

A

Yes

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25
Q

Is cross-resistance common for aminoglycosides?

A

No

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26
Q

How can bacteria become resistant to fluoroquinolones?

A
  • Alter DNA gyrase
  • Decreased uptake
  • Increased efflux
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27
Q

Is cross-resistance among quinolones common?

A

Yes

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28
Q

Bacteria that obtain ____ from the environment are resistant to sulfonamides

A

Folate

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29
Q

How can a bacteria become resistant to sulfonamides?

A

Altered dihydropteroate synthase

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30
Q

How can a bacteria become resistant to trimethoprim?

A

Altered dihydrofolate reductase

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31
Q

Why is cotrimoxazole resistance rare?

A

Bacteria must have simultaneous resistance to both sulfonamide and trimethoprim drug

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32
Q

What are some potential solutions to infections caused by resistant superbugs?

A
  • Knowledge about resistant infections
  • Infection control
  • Vaccination
  • Appropriate antibiotic use
  • Discover and develop new antibiotics
  • When treating, treat as early as possible and kill the pathogen
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33
Q

How is tuberculosis acquired?

A

Person-to-person transmission of airborne droplets of organisms from an active case to a susceptible host

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34
Q

What is the physical evidence of tuberculosis?

A

A tiny, fibrocalcific nodule at the site of infection (may or may not be present)

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35
Q

What is latent tuberculosis?

A

Positive tuberculin skin test but no disease

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36
Q

What is active tuberculosis?

A

Clinical signs and symptoms w/ radiographic and bacteriological evidence

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37
Q

What are signs and symptoms of tuberculosis?

A
  • Pulmonary cavitation
  • Myobacteria dissemination
  • Presence of bacteria in sputum
  • Malaise, anorexia, weight loss, fever
  • Increased sputum
  • Extrapulmonary sx (liver, bone marrow, spleen, kidneys, fallopian tubes)
38
Q

Is M. tuberculosis considered fast or slow growing?

A

Slow

39
Q

What is M. tuberculosis resistant to?

A

Drying, most antibiotics, and host killing

40
Q

M. tuberculosis has ____ survival

A

Intracellular

41
Q

What is the most important portion of M. tuberculosis for resistance?

A

Cell envelope

42
Q

What occurs in the primary infection of tuberculosis?

A
  • Most often asymptomatic
  • Regional lymph node spread and bacteremia
  • Infection is controlled w/ development of cellular immunity
  • Positive TST
43
Q

What effect does the tuberculosis disease have on the body?

A

Lowered immune defenses and possible re-infection

44
Q

Where does tuberculosis reactivation most often occur?

A

In lungs; can occur in lymph nodes, pleural space, kidneys, gut, and CNS

45
Q

If a px has ____ TB they will be infectious

A

Pulmonary

46
Q

Which px are more likely to have reactivated TB?

A

Px w/ weakened immune systems

47
Q

What is TB therapy based on?

A

Stage (latent or active)

48
Q

What are the first line drugs for TB?

A
  • Isoniazid
  • Rifampin
  • Pyrazinamide
  • Ethambutol
49
Q

Where is mycolic acid found?

A

Mycobacteria cell wall

50
Q

What are mycolic acids?

A

Beta-hydroxy fatty acids w/ a long alkyl side chain

51
Q

___ is the most important drug for TB tx and prophylaxis

A

Isoniazid

52
Q

What is the mechanism of isoniazid?

A

Inhibits mycolic acid synthetase => mycobacterial cell death

53
Q

What are adverse effects of isoniazid?

A
  • Hepatic toxicity
  • Peripheral neuropathy
  • Rash
54
Q

Is isoniazid bactericidal or bacteriostatic?

A

Bactericidal to actively growing bacilli

55
Q

What is significant about isoniazid?

A

A prodrug that is converted to active form by bacterial catalase peroxidase

56
Q

What is rifampin effective against?

A

Several gram positive and gram negative as well as M. tuberculosis

57
Q

What is the mechanism of rifampin?

A

Inhibits DNA-dependent RNA polymerase => inhibition of RNA synthesis and mycobacterial cell death

58
Q

Does rifampin bind mammalian RNA polymerase?

A

No

59
Q

What is pyrazinamide converted to and by which enzyme?

A

Converted to active pyrazinoic acid by pyrazinamidase

60
Q

What is the mechanism of pyrazinamide?

A

Inhibits mycolic acid synthesis => mycobacterial cell death

61
Q

What is pyrazinamide effective against?

A

Dormant and semi-dormant mycobacteria is acidic environments

62
Q

What is the mechanism of ethambutol?

A

Inhibits arabinosyl transferase => inhibition of arabinogalactan chain elongation, inhibition of mycobacterial cell wall synthesis, and reduction of mycobacterial cell growth

63
Q

Is ethambutol bacteriostatic or bactericidal?

A

Bacteriostatic

64
Q

What is isoniazid used for in the tx of TB?

A
  • Bactericidal in extracellular areas w/ high oxygen concentration
  • Important at preventing resistance by killing off rapidly growing bacilli
65
Q

What is rifampin used for in the tx of TB?

A

Only drug that is bactericidal in fibrotic areas

66
Q

What would be needed in rifampin wasn’t used?

A

18 months of tx

67
Q

Which drug is essential is more advanced stages of TB?

A

Rifampin

68
Q

What is pyrazinamide used for in the tx of TB?

A

Important in sterilizing semi-dormant bacteria

69
Q

When does pyrazinamide lose its activity?

A

As inflammation resolves

70
Q

What is ethambutol used for in the tx of TB?

A

Primarily used to prevent rifampin resistance when primary isoniazid resistance may be present

71
Q

When is ethambutol not used?

A

In renal failure and in children

72
Q

What is the goal of the intensive phase of TB tx?

A

Quickly kill the rapidly dividing organism to control disease and render px non-infectious and prevent emergence of drug resistance

73
Q

What is the goal of the continuation phase of TB tx?

A

Sterilize lungs by killing dormant and semi-dormant organisms to prevent relapse

74
Q

How long does each phase of TB tx last?

A
  • Intensive phase = 0-8 weeks

- Continuation phase = 2-6 months

75
Q

What drugs does the intensive phase include?

A
  • 4 drugs for 8 weeks
  • Normally 7 days a week, but minimum 5 days a week
  • Isoniazid, rifampin, pyrazinamide, and ethambutol (can be dropped if organism pansensitive)
76
Q

What drugs does the continuation phase include?

A

2 times/week isoniazid and rifampin

77
Q

What is the tx for latent tuberculosis?

A

Isoniazid daily for 9 months or rifampin daily for 4 months

78
Q

What is multi-drug resistant TB?

A

Resistant to rifampin and isoniazid and/or other drug

79
Q

When does multi-drug resistant TB most often occur?

A

In px w/ weakened immune systems (patients w/ HIV or immunosuppressed px)

80
Q

What is extensively-drug resistant TB?

A
  • Resistant to rifampin and isoniazid
  • Resistant to any quinolone
  • Resistant to any injectable 2nd line agent
81
Q

Why is extensively-drug resistant TB so bad?

A

Makes TB essentially untreatable

82
Q

How can a bacteria become rifampin resistant?

A

Alteration in DNA-dependent RNA polymerase

83
Q

What causes isoniazid resistance?

A

Decreased drug uptake

84
Q

What are the possible treatments when a px is isoniazid resistant?

A
  • Rifampin, pyrazinamide and ethambutol for 6-9 months
  • Rifampin, pyrazinamide, and streptokinase for 6-9 months
  • Rifampin and ethambutol for 12 months
85
Q

What causes pyrazinamide resistance?

A

Loss of pyrazinamidase, causing decreased conversion to pyrazinoic acid, so mycolic acid synthesis occurs and mycobacterial cells survive

86
Q

What causes ethambutol resistance?

A

Mutations in bacterial arabinosyltransferase gene, causing arabinogalactan elongation to continue, allowing mycolic acid synthesis and mycobacterial cells survive

87
Q

What is the tx for MDR-TB?

A
  • Combinations of 5-7 drugs:
  • Isoniazid, rifampin, pyrazinamide, ethambutol
  • Protein synthesis inhibitors (cycloserine, capreomycin, kanamycin)
  • DNA synthesis inhibitor (fluoroquinolones, aminosalicylic acid)
  • Metabolite synthesis inhibitor (ethionamide)
88
Q

What is the mechanism of bedaquiline?

A

Inhibits mycobacterium ATP synthase

89
Q

What is bedaquiline used for?

A

MDR-TB when in combination w/ rifampin and pyrazinamide

90
Q

Is bedaquiline useful against latent infections?

A

Unknown

Pharmacology - Fall (15 decks)

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