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Pharm Exam 3 > Anti-Microbial Drugs > Flashcards

Anti-Microbial Drugs Flashcards

1
Q

Group 1 Antibiotic Families (BacterioCIDAL)

A 
Penicillins
Cephalosporins
Vancomycin
Bacitracin
Aminoglycosides
Fluoroquinolones

Polymixin (only one that is non-cycle active)

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2
Q

Group 2 Antibiotic Families (BacterioSTATIC)

A 
Chloramphenicol
Tetracyclines
Erythromycin
Retapamulin
Quinupristin/Dalfopristin
Linezolid
Clindamycin
Sulfonamides
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3
Q

Vancomycin

A 
MOA: inhibits PG formation
Spectrum: Narrow G+ (especially staph)
Absorption/Distribution: need IV
Term: renal
Tox: nephrotoxic; hearing loss
Recent Resistance problem: resort to Linezolid or Quino/Dalfopristin
-NO CNS
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4
Q

Bacitracin

A

Inhibits PG formation
Narrow G+ spectrum
IV req’d
Nephrotoxin – LIMITED TO TOPICAL USE (often combined with other ABs in topical cream for G-‘s)

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5
Q

Mechanism of Action for Penicillin Family

A

Their B-lactam group allows them to act as a substrate for transpeptidase (PG cross-linker). They will inhibit cell wall synthesis.

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6
Q

Resistance to Penicillins

A

Penicillinase (aka a B-lactamase) produced by the bacteria will open the B-lactam ring and it will no longer be used as a substrate for transpeptidase

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7
Q

Penicillin G

A

NOT acid stable
Penicillinase sensitive
Narrow Spectrum G+

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8
Q

Phenoxymethyl Penicillin

A

acid stable
Penicillinase sensitive
Narrow Spectrum G+

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9
Q

Methicillin

A

NOT acid stable
Penicillinase RESISTANT
Narrow spectrum G+

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10
Q

Dicloxacillin, Oxacillin, Cloxacillion (DOC)

A

acid stable
Penicillinase resistant
narrow spectrum G+

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11
Q

Amoxicillin

A

acid stable
Penicillinase sensitive
BROAD spectrum (relative to Pen. G) especially for G-

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12
Q

Carbenicillin

A

IV req’d
penicillinase sensitive
MOST broad spectrum

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13
Q

MOA Beta-Lactamase Inhibitors (Clavulanic Acid or Tazobactam)

A

Prevent bacterial b-lactamases from opening the b-lactam ring in penicillin family antibiotics.

DO NOTHING BY THEMSELVES

Combined with other antibiotics for effect; i.e. “Augmentin” = Amoxicillin + Clavulanic Acid

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14
Q

Azlocillin, Ticarcillin, Piperacillin (ATP)

New members to penicillin family

A

broad spectrum
IV req’d
penicillinase sensitive

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15
Q

Antibiotics most effective against anaerobes

A

Imipenem, Clindamycin, 3rd gen. cephalosporins, piperacillins (ICCP)

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16
Q

MOA of cephalosporins

A

Also have a b-lactam ring; work like penicillins
Advantage = Resistant to penicillinase BUT still susceptible to other b-lactamases

ALSO have a much broader G- spectrum vs penicillins

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17
Q

Cephalosporin general generation patters

A

1st: similar to broad spectrum penicillins (G+)
2nd: more effective against G-
3rd: Less effective vs G+, but very effective against G-, anaerobes and CNS!

All Have bone marrow suppression and renal toxicity

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18
Q

Carbapenems

A 
Also B-lactam group
VERY broad spectrum: G+ G- and anaerobes
MUST BE combined with cillistatin to inhibit host renal enzyme catabolization
IV admin req'd
Resist B lactamase
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19
Q

Monobactams

A

Also B-lactam group
Broad spectrum G- but narrow spectrum G+ (important for G+ staph infections)

IV req’d

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20
Q

Name the B-lactam containing families (4 of em)

A

1) Penicllin
2) Cephalosporins
3) Carbapenems
4) Monobactams

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21
Q

Name the 4 “groups” of antibiotics that act on cell membrane

A

1) Polymixin
2) Nystatin
3) Amphotericin B
4) “-azoles” (antifungals)

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22
Q

Polymixin

A

UNIQUE: only bacteriocidal drug that will NOT be inhibited by bacteriostatic group because it is non-cycle active (binds and disrupts cell membrane)

Not good for oral: but used to decrease bowel flora prior to surgery

TOPICAL USE ONLY (really nephrotoxic)

Narrow spectrum G-: for pseudomonas, eye, skin, mucus membranes

23
Q

Nystatin & Ampho B (polyene group)

A

Bind ergosterol in cell membrane of fungii (thus selectively toxic, with little affinity for human cholesterol)

Ampho B given via IV with nephro toxicity

Nystatin is TOPICAL ONLY (severe nephrotoxicity)

24
Q

“-Azole” Antifungals

A

Inhibits 14-alpha-sterol demethylase: thus fungal specific for ergosterol synthesis

Can be given Orally

IMPORTANT: ALL are somewhat CYP450 mediated metabolized… thus will increased the half life of other drugs that require this enzyme for metabolism!

25
Q

Itraconazole

A

Low gastric pH enhances absorption (antacid decreases it)

Does NOT distribute to CNS

Excreted in bile and urine

26
Q

Fluconazole

A

Oral absorption pH independent

Renal excretion

DOES distribute to CNS (USE for CNS fungal infection!)

27
Q

5-Fluorocytosine

A

requires metabolism to de-aminated 5-fluorouracil (5-FU) for effect

Well absorbed orally

Distributes to CNS

Renal excretion/bone marrow suppression (will be seen again in cancer chemotherapy)

28
Q

Antibiotics that affect Nucleic Acids

A

Fluoroquinolones (ciprofloxacin & levofloxacin)
Rifampin
Nitrofurantoin

29
Q

Fluoroquinolones (ciprofloxacin & levofloxacin)

A

MOA: inhibition of gyrases/topoisomerases selective for bacteria (thus bacterioCIDAL)

Mostly act on G- bacilli (no anaerobes)

Some liver, some kindey excretion

Active in urine (thus good for UTIs)

Causes Cartilage damage! (avoid in those <17 years old)

30
Q

Rifampin

A

Inhibits RNA polymerase

more effective vs G+ vs G-

Absorption oral, IV, or IM

ORANGE tint to urine/bodily secretions!

Termination via liver (thus no need to modify dose for those who with renal insufficiency)

TERATOGENIC

31
Q

Drugs that act on the 30s Ribosomal Subunit

A

Aminoglycosides

Tetracyclines (“-cyclines”)

32
Q

Aminoglycosides

(Limited use due to: toxicity, rapid dev of resistance, and lack of oral absorption)

Includes: Gentamicin, Amikacin, Tobramycin, Netilmicin

A

MOA: 1st effect = Reduced (not stopped) protein synthesis

2nd effect: incorrect insertion of amino acids resulting in non-function proteins (thus bacterioCIDAL)

Broad spectrum: G- especially, and some G+

req’d IV

Renal excretion; still active in urine (thus can be used for UTIs)

Nephrotoxic, OTOTOXICITY (vestibular and auditory), also blocks NMJs

USE: G- bacilli (pseudomonas) klebdiella

Important: Resistance due to biolfilms (especially if using a sub-therapeutic dose)

33
Q

Tetracyclines

A
  • preferred is doxycycline for parenteral use
  • oxytetracycline best for preggers

MOA: inhibits access of aminoacyl tRNA to 30S ribosome… thus slowing protein synth (not stopping it)…thus bacterioSTATIC (compare to aminoglycosides!)

VERY BROAD SPECTRUM

Potential for SUPERINFECTION

phototoxicity

34
Q

Drugs that act on 50s Subunit (names and MOA)

A

Chloramphenicol
Macrolides (ie erythromycin)
Retapamulin
Clindamycin

MOA: inhibits peptide bond formation thus SLOWING protein synth, bacertioSTATIC

35
Q

Chloramphenicol

A

Broad spectrum-Treats Rikettsiae and antibacterial

Distributes well to CSF and TBW! – use for meningitis!!!

Resistance due to metabolism, lack of uptake and altered receptor

Liver metabolism (addition of glucuronic acid) thus DON’T use in infants! causes CV problems! Prolonged levels due to lack of metabolism-heptatoxicity

36
Q

Bone Marrow Toxicity with Chloramphenicol

A

Toxic = normocellular appearance, anemia in blood, DOSE-RELATED, toxic ONLY during treatment, recovery occurs

VERSUS

Aplastic: hypoplastic/aplastic appearance in marrow, pancytopenia in blood, NOT DOSE RELATED, toxic days/months after treatment, common symptoms = purpura and hemorrhage! OFTEN FATAL!

37
Q

“Macrolide” anibiotic members + MOA

A

1) Erythromycin
2) Clarithromycin
3) Azithromycin
4) Telithromycin
(E-CAT)

MOA: Binds 50S subunit; inhibits peptide bond formation, thus slow down protein synth, thus bacterioSTATIC

38
Q

Erythromycin

A

Similar spectrum to Pen G: mostly G+, some G-; notably ===> against penicillinase-producing organisms! (mycoplasma!)

Oral absorption

VERY LITTLE TOXICITY

Note: clarithromycin & azithromycin slightly more broad spectrum and better absorption than erythro

39
Q

Telithromycin

A

well absorbed orally

metabolized in liver

Adverse side effects: headache, blurred vision, altered taste perception… can cause SEVERE hepatic toxicity… use limited to serious respiratory infections!

40
Q

Retapamulin

A

MOA: recall a 50s binding; thus inhibits peptide bond formation ALSO blocks binding of tRNA to ribosome (UNIQUE!)… thus slows protein synth in 2 ways but still bacterioSTATIC

TOPICAL use only– good for strep and staph

41
Q

Clindamycin

A

active against anaerobes!

does not go to CSF

Metabolized in liver

main toxic effect = butt pee (aka diarrrrheaaa)

42
Q

4 New drugs to treat vancomycin resistant bugs and their MOA

A

“Quality Dairy Likes TouchDowns” (Quinupristin/Dalfopristin, Linezolid, Tedizolid, Dalbavancin)

MOA: most act at 50s Subunit, (thus all bacterioSTATIC) excepet dulbavancin prevents cross-linked wall

43
Q

Quinupristin/Dalfopristin

A

G+ staph and strep, especially vanco-resistant

IV req’d

Adverse: edema, thrombophlebitis @ infusion site, arthralgia and myalgias

44
Q

Linezolid

A

same as Q/D but MORE broad spectrum

MOA: blocks formation of 70S (50S plus 30S)

Adverse: thrombocytopenia (must monitor platelets counts)

45
Q

Tedizolid

A

Narrow spectrum G+

VERY important for methicillin resistant staph. aureus (MRSA)

Better than dulbavancin because can be given orally

46
Q

Dulbavancin

A

Very important for MRSA as well as Tedizolid

BUT req’d IV

MOA: binds D-alanyl-D-Alanyl in cell wall to prevent cross-linking

47
Q

Antibiotics affecting metabolism (antimetabolites)

A

*she tried fucking U
Sulfonamides (sulfa drugs)
Trimethoprim
5-Fluorocytosine ===> 5-Fluorouracil (5-FU)

48
Q

Sulfa Drugs

A

MOA: analogs of p-aminobenzoic acid – required for synthesis of Folic acid (bacteria selective because they must synthesize folic acid versus humans who just must ingest vitamin B9)

*Sulfisoxazole has highest solubility at all pH’s in kidney

Broad G+ and G-; resistant prevalent

BacterioSTATIC

Does get to CNS!

Toxicity: crystaluria (thus very dependent on host hydration and urine pH!!!… can be very effective against UTIs though!)

49
Q

Concept of Sequential Inhibition

A

Applies to folic acid synthesis in bacteria… there are many required enzymes to make FA… thus if you only block one (via competitive inhibition) a certain intermediate will build in concentration overcoming the inhibition…

BUT, if you block at 2 enzymes in a row… it becomes MUCH harder for the two intermediates to build high enough concentrations to overcome 2 consecutive competitive inhibitors!

50
Q

Trimethoprim-Sulfamethoxazole

A

example of overcoming sequential inhibition… they both block different enzymes in the synthesis of folic acid

Sulfas block Dihydropteroate synthetase (PABA—>Folate)
Trimethoprim blocks dihydrofolate reductase (Folate—->tetrahyrofolate)

51
Q

Flucytosine

A

MOA: metabolized by the FUNGI to 5-FU blocking nucleic acid synthesis

Gets to CNS

Active in urine (useful for UTI)

Fungal-selective for 2 reasons:
1) requires cytosine-specific permeases to get into cells… they are found only in fungal membranes

2) 5-FC is deaminated to 5-FU by a cytosine deaminase that is NOT present in mammalian cells

5-FU is then converted to 5-FdUMP which inhibits thymidylate synthetase blocking DNA synthesis

52
Q

Urinary Tract Antiseptics

A

Nitrofurantoin

Methenamine

53
Q

Nitrofurantoin

A

MOA: bacteria selective because bacterial enzymes will more rapidly reduce nitrofurantoin to intermediates which damage DNA compared to mammalian enzymes

Renal Excretion, active in urine

TURNS URINE BROWN! (not a real concern)
nausea vomiting diarrhea headache and pulmonary fibrosis (rare)

54
Q

Methanamine

A

MOA: hydrolized to formaldehyde and ammonia

Spectrum: G+ and G-
Oral is good

BacterioCIDAL in acid
Bacterio STATIC in alkaline

Thus usually administered with mandelic acid to lower urinary pH to be bacteriocidal… DON’T use with sulfa drugs because the low pH will increase risk of urine crystals

Pharm Exam 3 (3 decks)

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