Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Micro > 6/7 antibiotics and antimetabolites > Flashcards

6/7 antibiotics and antimetabolites Flashcards

1
Q

3 classes of antimicrobial agents

A
  1. antiseptics: no selective toxicity, topical/surfaces, chlorhexidine mouthwash
  2. sulphonamides = antimetabolites
  3. antibiotics = produced by microorgs to combat each other
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

perfect antibiotic, 8 traits

A
  1. selective toxicity
  2. bacteriocidal
  3. long in vivo half life
  4. good tissue distribution
  5. low plasma protein binding
  6. oral and parental admin possible
  7. limited drug interactions
  8. eventual elimination

S B L G L O L E
super big large giant lion owns little elephant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

pneumoic for 8 perfect traits

A

super big large giant lion owns little elephant

sel.tox, bacteriocidal, long in vivo, good tissue distrib, low pp binding, oral/parental admin, limited drug ineraction, eventual elim.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

empirical therapy uses what tests

A
  1. diffusion: biggest zone of inhibition means most bacterial susceptibility
  2. dilution: clear in medium = MIC; no growth of the clear ones on plate with no abx = MBC
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

5 big problems with abx use

A
  1. side effects
  2. harm commensal flora and allow pathogenic bacteria space to grow
  3. resistance
  4. allergy
  5. $$$
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

odontogenic infection

A

bacteria gains access to pulp

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

periapical infection

A

spread of infection from root canals into periapical region of alveolar bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what was the nasty puffy neck person pic

A

periapical absess (from root to bone)

all the light areas in the X ray = infection spread throughout alveolar bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

periapical infection 1st line of treatment

A

-debridement
-endo therapy
-extraction
^^^mechanical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

when do you use abx for periapical infection

A
  • when infection has spread beyond alvoelar bone

- use mechanical methods in conjunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

when do you use abx for periodontal infection?

A
  • when mechanical/home care does not resolve
  • when immunocompromised
  • early onset periodontitis
  • systemic disease that predisposes to periodontitis
  • severe perio infection (absess etc)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what situations warrant abx prophylaxis? (3)

A
  1. immunocompromised (chemo, radiation, immundeficiency disease)
  2. facial/skull fracture
  3. patients at risk for IE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

infective endocarditis

A
  • platelets adhere to heart valve abnormalities to form sterile thrombus (sterile vegetation)
  • bacteria introduced into bloodstream then colonize the thrombus (tooth extraction, perio therapy)
  • heart valves scar and thicken (vegetation)
  • emboli (clots) form and break off, or just gets so big that CHF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

bacteremia can also result from….? (non invasive procedures)

A
  • brushing, flossing
  • eating
  • perio lesions from poor oral hygiene
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

5 ways bacteria become resistant

A
  1. decreased entry
  2. efflux pump
  3. enzymatic inactivation/modification of drug by bacteria
  4. bypass pathway: drug has non susceptible pathway that does same fxn
  5. altered target site: bacteria modifies wahtever cell of its own that is the drug target
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

peptidoglycan composition

A
  • parallel chains of NAM adn NAG that are CROSS LINKED by short amino acid chains
  • G pos cells have more of it
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

cell wall synthesis inhibitors

A
  1. B-lactams: binds PBP’s which make cross links
  2. glycopeptides: bind directly to growing chain
  • bacteriocidal because they block peptidoglycan synthesis
  • selective toxicity bc we do not have peptidoglycan
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

beta-lactams

A

penicillin, amoxocillin, methicillin (**narrow spectrum, insensitive to some b-lactamases)

cephalosporins (1st only Gpos but now G neg as well)

  • allergies common
  • res = alter PBP, b-lactamases cleave b-lactam ring
  • oral, IV, intramuscular admin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

beta-lactam resistance and get aroudn it how

A
  • alter PBP’s
  • b-lactamases cleave b-lactam ring

**augmentin = potassium clavulanate + amoxicillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

beta-lactamase mechanism

A

-block action of PBP’s (transpeptidase) which cause cross linking between NAM subunits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

glycopeptides

A

(vancomycin, teicoplanin – Gpos only)

  • mech: bind directly to growing peptidoglycan chain
  • skin rash, oto/nephrotoxicity (used for IE prophylaxis)
  • res: Gneg inherently resistant; alter NAM/NAG terminal aa
22
Q

how does vancomycin work

A

bind D-ala-D-ala terminal sequence of peptidoglycan on G pos cells (glycopeptide)

23
Q

protein synthesis inhibitors (6 groups)

A
  • largest group
  • target rRNA: 30S, 50S SU
  1. aminoglycosides
  2. tetracyclines
  3. macrolides
  4. lincosamides
  5. chloramphenicol
  6. fusidic acid

**different drugs target different steps of translation

24
Q

what is the target for the largest variety of abx?

A

protein synthesis – so many steps and so much involved

25
Q

aminoglycosides

A

strepto, genta, kana, neo, turboMYCIN

  • mech: irreversibly bind 30S SU, prevent initiation
  • broad spec, bacteriocidal (only target aerobes, not intracellular/anaerobic bacteria)
  • topical
  • SE: nephro/ototoxic–do not administer sysmetically, adn monitor if you do
  • res: efflux, decreased perm, alter 30S
26
Q

aminoglycosides mechanism

A

(kana, strepto, ganta, neo, turbo MYCIN)

  • irreversibly bind 30S to prevent inititiaon of translation
  • bacteriocidal
  • does not work on anaerobic/intracellular bacteria
27
Q

aminoglycosides admin/SE

A
  • topical usually
  • SE = nephro/ototoxicity
  • so do not administrer systemically (except to kill G(-) intestinal flora pre surgery or prophylaxis for IE)
  • if systemic, MONITOR blood levels
28
Q

tetracyclines

A

tetra/doxyclycline

  • REVERSIBLY binds 30S to prevent tRNA docking
  • bacteriostatic, broad spectrum
  • oral admin
  • used in mouthwash
  • SE: GI distress adn discolors teeth in kids (do not give to them)
  • Res = high; efflux adn altered 30S
29
Q

tetracyline mech

A

bind reversibly to 30S to prevent tRNA docking, b.static and broad
(tetra and doxyclycine)

30
Q

Macrolides and Lincosamides

A
  • reversibly bind 50S to prevent elongation
  • bacteriostatic, but b.cidal in high doses
  • broad spec, so good alternative if penicllin allergy
  • oral, very safe
  • nausea
  • res = alter 50S, efflux, decrease perm, inactiveate drug
31
Q

macrolides

A
  • erythro/azythromycin
  • reversibly binds 50S to block elongation by blocking ribosomal translocation
  • b.static (unless high dose) and broad, good penicllin alternative
  • erythromycin is one of safest drugs ever
32
Q

lincosamides

A
  • clindamycin
  • reversibly binds 50S to prevent elongation by preventing peptide bond formation
  • ANAEROBIC INFECTION drug of choice
  • broad
  • bstat (unless high dose)
33
Q

lincosamide vs macorlide

A

both reversibly bind 50S to prevent elongation

  • lincosamide = clindamycin; prevents peptide bond formation **anaerobe
  • macrolide = erythro/azythromycin; prevent ribosomal translocation
34
Q

macrolide mech

A

block ribosomal translocation (bind 50S)

35
Q

last resort drugs

A
  1. chloramphenicol

2. fusidic acid — not avilable in USA

36
Q

chloramphenicol

A
  • irreversibly binds 50S, broad spectrum
  • potentially fatal, use only when infection is life threatening
  • fatal aplastic anemia adn gray baby syndrome
37
Q

fusidic acid

A

binds elongation factor

toxic to mamalian ribosomes? not available in USA

38
Q

3 types of abx that inhibit nucleic acid synthesis

A
  1. nucleotide synthesis (sulfonamide and trimethoprim)
  2. DNA rep (quinolones)
  3. mRNA synthesis (rifamycins)
39
Q

sulfonamide & trimethoprim

A

ANTIMETABOLITES - inhibit synthesis of THF (tetrahydrofolate) which is needed for purine (AA) synthesis

admin = oral
SE = allergy, nausea, vomit, headache, depression, dizzy
40
Q

pathway of sulf/trimeth

A
  1. PABA, glutamate, pteridine-H2 convert to DHF (folic acid), catalyzed by DIHYDROPTEROATE SYNTHETASE
    ^^microorgs only
  2. DHF/folic acid is catalyzed by DIHYDROFOLATE REDUCTASE to make THF
  3. THF then made into purine
41
Q

sulfonamide

A
  • synthetic structural analogs of PABA, competitively inhibit dihydropteroate synthetase to block DHF (folic acid) synthesis
  • we dont make folic acid (eat it) so not toxic to us
  • bstatic
  • broad (protozoa, intracellular)
  • res = overproduce PABA or alter dihydrop.synthetase target
42
Q

trimethoprim

A
  • synthetic pyridine analog (analog of pteridine portion of DHF)
  • competitively inhibits bacterial DHF reductase (50000-100000x higher affinity for bacterial enzyme than human)
  • broad
  • res = altered DHF reductase (overproduce, mutate, 2nd enxyme) or decreased perm
43
Q

when are trimethoprim adn sulfonamide most effective (bacteriocidal)

A

in combo. synergistic.
BACTERIOCIDAL when in combo

sulfamethoxazole + trimethoprim = bactrim-spectra = co-trimoxazole = SXT

44
Q

quinolones

A

nalidixic acid, ciprofloxacin

  • inhibit DNA gyrase, so the bacteria cannot supercoil its DNA and DNA rep cannot happen
  • bacteriocidal
  • moderate spectrum, mostly Gneg
  • oral admin
  • SE = GI, rare…neurotoxicity or photosensitivity
  • res = DNA gyrase mutation or decreased perm
45
Q

quinolone example

A

nalidixic acid

ciprofloxacin

46
Q

rifamycins

A
  • bind RNA polymerase to prevent transcription initiation
  • bbacteriocidal, broad
  • oral admin
  • minimal SE
  • res = mutant RNA pol beta subunit
47
Q

names of b-lactams

A 
penicillin
amoxilccin
ampicillin
nafcillin
methicillin

and cephalosporins

48
Q

aminoglycosides, names

A 
streptomycin
kanamycin
neomycin
tobramycin
gentamycin
49
Q

macrolides and lincosamides, names

A

macrolide = erythromycin and azythromycin

lincosamide = clindamycin (**anaerobic killer)

50
Q

quinolone names

A

levofloxin
ciprofloxixin
nalidixic acid

Micro (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions