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antibacterials Flashcards

1
Q

invaders

A
  • bacteria (protozoa- no nuclei)
  • fungi (eukaryote)
  • protozoa (eukaryote)
  • helminth (eukaryote)
  • viruses
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2
Q

chemotherapy

A

drugs selectively toxic to invader
- minimal effect on host

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3
Q

bacterial infection example

A

necrotizing fasciitis (flesh eating disease)

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4
Q

necrotizing fasciitis

A
  • break in skin, nutrients, warm and moist environment for bacteria
  • bacteria release chemicals that kill human cells
  • antibiotic treatment
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5
Q

prokaryotic cells

A
  • DNA not in nucleus
  • adaptable
  • wide range of environments like temps and levels of oxygen(diff types)
  • pathogenic and non-pathogenic
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6
Q

what is infection

A

invasion and multiplication of organisms that lead to untoward consequences
- from foreign bacteria or normal flora

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7
Q

colonization

A
  • normal flora that live on/in our body
  • non-pathogenic
  • if circumstances change in person, colonization can become infection
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8
Q

bacteria shapes

A
  • cocci (circle)
  • bacilli (rods)
  • strepto (chains)
  • staphylo (clumps)
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9
Q

bacterial cell wall

A
  • outside plasma membrane
  • structural support (internal osmotic pressure)
  • protection
  • gram positive or gram negative (key difference for drug therapy)
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10
Q

gram positive cell wall

A
  • thick peptidoglycan layer (50%)
  • gram stain trapped in wall, gram stains purple
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11
Q

gram negative cell wall

A
  • thin peptidoglycan layer (5%)
  • has outer membrane
  • less gram stain trapped
  • harder to treat bc outer membrane is a barrier to antibiotics
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12
Q

gram positive bacteria example

A

staphylococcus aureus

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13
Q

gram negative bacteria example

A

escheria coli

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14
Q

narrow spectrum antibacterials

A

selective against one class of bacteria
- ex. only gram positive

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15
Q

broad spectrum antibacterials

A

effective against both classes of bacteria (g-ve and g+ve)
- can affect healthy bacteria you do not want to get rid of

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16
Q

bactericidal

A

directly lethal to bacteria (kill)

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17
Q

bacteriostatic

A

slow bacterial growth
- host immune system helps body control/eliminate bacteria

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18
Q

superinfection (suprainfection)

A
  • new microbes take over when antibacterials kill normal flora
  • new microbes are resistant to drug action and difficult to treat
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19
Q

opportunistic infections

A
  • infections that would normally not harm person
  • existing colonization become infections
  • antibiotic took out normal flora so new infections have no competition
  • common in immunocompromised
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20
Q

antibacterial drug resistance

A

bacteria less susceptible to drug action
- bacteria pumps drugs out
- enzymes break down/change drug

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21
Q

what causes drug resistance (mutation)

A
  • choosing wrong antibiotic
  • dose too low
  • dose not taken long enough
  • improper use (treat virus)
  • prophylactic use (animal feed)
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22
Q

host factors affecting drug choice

A

age, allergies, organ health, pregnancy, site of infection, general health

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23
Q

antibacterials mechanism of action

A
  • disruption of metabolic reactions
  • interference with cell wall synthesis
  • interference with protein synthesis
  • interference with DNA replication/transcription mechanisms
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24
Q

antimetabolite example

A

sulfonamides
- sulfamethoxazole

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25
Q

sulfonamide characteristics

A
  • broad spectrum
  • bacteriostatic
    -prevent synthesis of folic acid
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26
Q

sulfonamide (sulfamethoxazole) mechanism of action

A

inhibit enzymes so bacteria can’t make folic acid (DNA/RNA), cells can’t replicate

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27
Q

sulfonamide (sulfamethoxazole) indications

A
  • UTI
  • otitis media
  • upper resp tract infections
  • malaria
  • chlamydia
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28
Q

what drug is sulfamethoxazole combined with? why?

A

trimethoprim
- makes more effective bc stops at 2 spots in folic acid pathway

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29
Q

contraindications

A
  • allergies (to all sulfa drugs)
  • pregnancy (birth defects, increase fetal bilirubin)
  • breastfeeding
  • infants < 2 mths
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30
Q

sulfonamide adverse effects

A
  • skin allergies (hypersensitivity, steven-johnson syndrome, photosensitivity)
  • bone marrow depression (agranulocytosis, thrombocytopenia, aplastic anemia)
  • nausea and vomiting
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31
Q

steven-johnson syndrome

A

swelling and rash of mucosal membranes

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32
Q

sir alexander fleming findings

A

mold growing on growth plate made chemical that kept bacteria away (starting point of antibacterial drugs)

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33
Q

beta lactam antibacterial characterstics

A
  • inhibit cell wall enzyme responsible for peptidoglycan synthesis (stop cell wall)
  • bactericidal
  • beta lactam ring is effective part of drug
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34
Q

groups of beta lactam drugs (4)

A
  • penicillins
  • cephalosporins
  • monobactams
  • carbapenems
35
Q

penicillins categories

A
  • naturally occuring
  • semi-synthetic
36
Q

naturally occuring penicillins

A
  • penG (IM, IV)
  • pen V (PO)
  • narrow spectrum
  • sensitive to beta lactamase (drug resistance)
37
Q

semi-synthetic penicillins

A
  • beta-lactamase resistant (cloxacillin)
  • broader-spectrum/aminopenicillins (ampicillin, amoxicillin (PO)
  • extended spectrum/antipseudomonal penicillins (ticarcillin, piperacillin)
38
Q

penicillin mechanism of action

A
  • inside cell bind to proteins
  • normal cell wall synthesis disrupted
  • bacterial cells rupture
39
Q

drug resistance to penicillin

A
  • enzymes (beta lactamases) can split beta lactam ring so drug ineffective
40
Q

how to stop penicillin resistance

A

b-lactamase inhibitors
- stop enzymes
- ex. clavulanic acid

41
Q

penicillin indications

A

g+ve bacteria
- broad/spectrum spectrum types kill g-ve

42
Q

penicillin adverse effects

A
  • GI problems (disturb normal gut flora)
  • allergic reactions (rashes, edema, can be fatal)
43
Q

cephalosporin characteristics

A
  • semisynthetic
  • b-lactam
  • bactericidal
  • divided into groups (generations)
44
Q

changes in cephalosporin generations

A
  • increased permeability to g-ve cell wall
  • increase stability against b-lactamases
45
Q

1st gen

A
  • for surgical prophylaxis, UTIs, otitis media
  • cefazolin: good for g+ve (IV)
  • cephalexin (PO)
  • cefadroxil
46
Q

2nd gen

A
  • good g+ve coverage
  • better g-ve coverage than 1st gen
  • cefuroxime (po) (surgical prophylaxis)
  • cefoxitin (IV & IM)
47
Q

3rd gen

A
  • broader spectrum (better against g-ve)
  • cefotaxime (IV & IM) (passes meninges and diffuses into CSF to treat CNA infections like meningitis)
  • cefixime (PO - best oral cephalosporin against g-ve)
48
Q

4th gen

A

broader spectrum
- especially g+ve
- cefepime

49
Q

5th gen

A

ceftaroline
- MRSA infections

50
Q

cephalosporin adverse effects

A
  • similar to penicillins
  • patients with history of allergy to penicillin may have cross hypersensitivity
51
Q

carbapenems characteristics

A
  • broad spectrum
  • good for mixed infections
  • not MRSA
  • last resort drug!!!
  • all parenterally given
52
Q

carbapenems example

A

imipenem

53
Q

imipenem combination drug

A

imipenem-cilastatin
- inhibits breakdown of imipenem in kidney

54
Q

carbapenems drug resistance

A
  • carbapenem-resistant bacteriaceae
  • enzymes: klebsiella pneumoniae caarbapenemase and new dehli metallo beta lactamase)
55
Q

macrolides (large molecules) example

A
  • erythromycin
  • azithromycin
  • clarithromycin
56
Q

macrolides mechanism of action

A

inhibit protein synthesis
- 50s ribosome

57
Q

macrolides characteristics

A
  • broad spectrum
  • bacteriostatic (some bactericidal with higher concentration)
58
Q

macrolides indications

A
  • patients allergic to b-lactam antibacterials
  • penicillin resistant bacteria
  • opportunistic infections - HIV/AIDs (azithromycin and clarithromycin)
  • infections of respiratory, skin, soft tissue
59
Q

macrolides adverse effects

A
  • GI disturbances
  • provoke cardiac dysrhythmia (long Q-T)
  • narrow therapeutic index of azithromycin and clarithromycin (fwer drug-drug interactions, little to no inhibition of CYP enzymes = increased concentration)
60
Q

tetracylines (group)

A
  • tetracycline
  • doxycycline
  • minocycline
  • demeclocycline
61
Q

tetracyclines charactersitics

A
  • very broad spectrum coverage (first drug to be broad spectrum!)
  • bacteriostatic
  • PO
62
Q

tetracycline mechanism of action

A

inhibit protein synthesis (30s ribosome)

63
Q

tetracycline interactions

A
  • bind to metal ions (Ca, Mg, iron, aluminum)
  • milk products, supplements, laxatives, antacids, iron salts
  • form insoluble complexes = chelation which cannot be absorbed
64
Q

tetracycline contraindications

A
  • pregnancy
  • breastfeeding
  • children < 8
65
Q

tetracycline adverse effects

A
  • strong affinity to calcium (bind to and discolour teeth)
  • slow fetal skeletal development
  • GI disturbances (alterations in GI flora)
66
Q

alteration of intestinal flora may result in:

A
  • superinfection
  • diarrhea
  • c difficile/colon infection (fecal transplant)
  • photosensitivity
  • can be antagonist to bacteriocidal antibacterials
67
Q

aminoglycosides (amino + sugar) characteristics

A
  • natural and semisynthetic
  • produced from streptomyces
  • first antibacterial against g-ve
  • bactericidal
68
Q

aminoglycosides mechanism of action

A
  • inhibit protein synthesis (30s)
69
Q

aminoglycoside example

A

gentamicin

70
Q

aminoglycoside indications

A
  • g-ve
  • often used synergistically with another antibacterial
71
Q

aminoglycoside administration route

A
  • poorly absorbed through GI tract (IV mainly or IM)
  • only give po to treat GI infection
72
Q

how to minimize aminoglycoside toxicities?

A
  • do not give next doses until plasma concentration levels very low
  • blast to high concentration then wait until low concentration to do it again
  • check with blood test
73
Q

aminoglycoside adverse effects

A
  • irreversible ototoxicity (inner ear)
  • reversible nephrotoxicity (kidney) (extreme in neonates and pre-existing kidney problems)
74
Q

aminoglycoside interactions

A

increased nephrotoxicity risk when taken with:
- vancomycin (antibiotic)
- cyclosporine (immunosuppressant)
amphotericin B (antifungal)

75
Q

quinolones/fluoroquinolones example

A

ciprofloxacin (very effective - PO)

76
Q

quinolones characteristics

A
  • bactericidal
  • broad spectrum
77
Q

quinolones mechanism of action

A

alter bacteria DNA
- transcription inhibitors

78
Q

quinolones indications

A
  • UTI (e coli)
  • anthrax
79
Q

quinolones adverse effects

A
  • GI: nausea, vomiting , diarrhea
  • skin: rashes
  • CNS: headache, dizziness
80
Q

quinolones interactions

A
  • drug-drug: cyp inhibition means less drug metabolism and higher level of drug concentration (theophylline, warfarin)
  • oral absorption reduced by: antacids, iron, zinc, calcium
81
Q

vancomycin mechanism of action

A

inhibit cell wall synthesis

82
Q

vancomycin characteristics

A
  • bactericidal
  • drug resistance increasing
  • last resort drug
83
Q

vancomycin administrations

A
  • IV: MRSA and g+ve bacteria
  • PO: GI problems like c diff
84
Q

vancomycin adverse effects

A
  • flushing syndrome (rly red face and chest from IV too fast)
  • nephrotoxicity
  • ototoxicity
  • phlebitis (inflamed vein at injection)

pharm (15 decks)

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