Pharm Test 4

Front 1

bacteriocidal

Back 1

Bactericidal typically has more rapid effect and less likely to induce resistance (tend to target cell wall or activate autolytic enzymes; i.e., penicillins
irreversible inhibitors are usually bactericidal (streptomycin)

Front 2

bacteriostatic

Back 2

Bacteriostatic relies heavily on competent immune response (tend to target metabolic pathways; i.e., sulfonamides); Also, reversible inhibitors of protein synthesis are often bacteriostatic (tetracyclines)

Front 3

MIC

Back 3

MIC (minimal inhibitory concentration-used most frequently): Concentration of drug required to inhibit growth of the pathogen.
--inc concentration the time to inhibit is decreased ---concentration dependent

Front 4

MBC

Back 4

MBC (minimal bactericidal concentration): Concentration required to kill the pathogen

Front 5

susceptibility testing

Back 5

-In vitro testing to confirm susceptibility to antimicrobial agents, ideally, to a narrow spectrum drug

Front 6

PAE

Back 6

Post-antibiotic effect (PAE)- give drug, after it is taken away then inhibition cont for a time; time required for the bacteria to return to log growth following drug withdrawal

The PAE in vivo is considerably longer than in vitro due presumably to post-antibiotic leukocyte enhancement (PALE) and exposure of bacteria to subinhibitory drug concentrations. Aminoglycosides and quinolones (once-daily) . have concentration-dependent PAE. For instance, aminoglycosides remain effective for some time after serum levels of the drug drop below the MIC of a given organism.

Front 7

why would you give IV antibiotics?

Back 7

critically ill, bacterial meningitis, endocarditis, N/V, gastrectomy

pharmacokinetics are pretty much the same orally or parenterally

Front 8

pharmacokinetics or oral vs parenteral antibiotics

Back 8

they are similar no matter what. a few exceptions for IV

Front 9

when are pharmacokinetics altered? what patients?

Back 9

Renal or hepatic insufficiency, Burns, CF, Elderly, neonates, pregnancy; may need to alter dosing but don’t necessarily HAVE to change

Front 10

what happens when vancomycin and penecillins are given with an aminoglycoside?

Back 10

synergystic effect instead of just bacteriostatic also bacteriocidal

Front 11

surgical prophylaxis

Back 11

Ab should be specific for common surgical wound pathogens (not broad spectrum), Proven efficacy in clinical trials; Concentration > MIC at time of incision, Single dose , Cefazolin and cefoxitin

Front 12

name the cell wall synthesis inhibitors

Back 12

Penicillins, β-lactamase inhibitors*, Cephalosporins, Monobactams, Carbapenems

Front 13

PBP

Back 13

Penicillin-binding proteins (PBP); NOT static; collective term for bacterial enzymes responsible for assembly, maintenance and regulation of the peptidoglycan portion of the cell wall, β-lactam Abs covalently bind PBP, Inhibition of PBP-1 prevents cross-linking of peptidoglycan, whereas, inhibition of PBP-2 results in loss of rod shape

Front 14

peptidoglycan

Back 14

-Linear strands of two alternating amino sugars which are crosslinked by a peptide chain.; Linkage is catalyzed by a transpeptidase, Penicillin irreversibly binds at the active site of the transpeptidase , It mimics the residues that would normally bind to this site.
it gives rigid support, portects aginst osmotic pressure

Front 15

pharmacokinetics of penicillins

Back 15

some are acid stable others are acid labile; Widely distributed, except not typically found in brain, prostatic secretions or intraocular secretion. Enter the CNS when meninges are inflammed.
they rely on the kidney for GFR and RTA; probenicid used to prolong HL

Front 16

penecillins can NOT be used in what dysfunction/disease

Back 16

renal dysfunction

Front 17

what is used to prolong HL in penicillins?

Back 17

probenecid

Front 18

name 2 long acting penecillins for IM

Back 18

Procaine penicillin G and benzathine penicillin G

Front 19

side effects of penicillin

Back 19

Hypersensitivity-Degradation products of penicillin combine with protein to form antigenic compounds; IgE mediated response
Rash , Nephritis, Serum sickness, Anaphylactic shock

Front 20

why are cephalosporins better than penicillins?

Back 20

More stable than penicillins (highly resistant to penicillinase) and less likely to cause hypersensitivity reactions,
Renal excretion-Except ceftriaxone which is excreted in bile; dose modification in renal dysfucntion

Front 21

Divided into 4 generations based on antimicrobial spectrum cephalosporins

Back 21

1st primarily active against most gram-positive cocci (not MRSA or enterococci) and some gram-negative organisms; 2nd-4th increased activity against Gram-negative bacilli

; as inc generation inc effect and strength against bugs

Front 22

cephalosporin Cross-sensitivity w/ penicillins

Back 22

-If mild reaction to penicillin then cephalosporins usually tolerable, If severe reaction to penicillin then cephalosporins contraindicated

Front 23

how do bacteria get resistance to B lactams?

Back 23

structural differences in PBPs, recombination of PBP genes of different species resulting in PBPs with low affinity for antibiotic; Efflux pumps; ↓ entry of the drug into bacteria through the outer membrane porins-In gram-negative bacteria the PBP are very near the cell surface thus more readily accessible , In gram-negative bacteria the outer membrane is often an impenetrable barrier to some antibiotics. However, hydrophilic antibiotics diffuse through aqueous channels created by proteins called porins.
P aeruginosa is intrinsically resisitant to many antibiotic b/c of a relatively low number of hightly-perimeable porins

Front 24

penicillin G

Back 24

Narrow Spectrum Penicillin Cell wall synthesis inhibitor; IRREVERSIBLY binds the active site of transpeptidase Acid-stable in large doses (oral)
Think Gram (+); CNS when meninges inflamed
Use with 3rd gen. cephalosporin or vancomycin until sure of PCN-sensitivity.

Hypersensitivity: degradation products of PCN combine w/protein = IgE mediated response w/rash, nephritis, serum sickness, Anaphylactic shock Elimination=kidneys

Used in elderly due to lower acid content
treats: Syphilis (Treponema pallidum) spirochete ; Meningitis (Meningococci) (-); Pneumonia (Pneumococci) (+)

Front 25

penicillin V

Back 25

Narrow Spectrum Penicillin Cell wall synthesis inhibitor;
IRREVERSIBLY binds the active site of transpeptidase Acid-stable (oral) Think Gram (+)
CNS when meninges inflamed Hypersensitivity reaction Elimination=kidneys
treats: Pharyngitis (Streptococcus pyogenes) (+)

Front 26

procaine Penicillin G

Back 26

Long-acting combination; penicillin; Cell wall synthesis inhibitor;
IRREVERSIBLY binds the active site of transpeptidase; Combined with Probenecid; competes w/ penillin for organic acid transporter IM
treat: Think Gram (+);
CNS when meninges inflamed Hypersensitivity reaction Elimination=kidneys

Front 27

benzathine penicillin G

Back 27

Long-acting combination Penicillin Cell wall synthesis inhibitor; IRREVERSIBLY binds the active site of transpeptidase; Combined with Probenecid; competes w/ penillin for organic acid transporter IM
tx: Think Gram (+);
CNS when meninges inflamed Hypersensitivity reaction Elimination=kidneys

Front 28

diclocillin

Back 28

Penicillinase resistant Penicillin IRREVERSIBLY binds the active site of transpeptidase; Acid stable (ORAL)
tx: Think Gram (+);
Osteomyelitis (Staphylococci);
Endocarditis (Staphylococci);
Skin/soft tissue infections (Staphylococci) Less effective than other PCNs; Use ONLY if bugs make penicillinase (PCN-resistant; MRSA)
Hypersensitivity reaction Elimination=kidneys;
Vancomycin is DOC for PCN-resistant bugs;
NOT for GRAM (-)

Front 29

nafcillin

Back 29

Penicillinase resistant Penicillin IRREVERSIBLY binds the active site of transpeptidase; PARENTERAL (IV) acid labile
tx: Think Gram (+);
Osteomyelitis (Staphylococci);
Endocarditis (Staphylococci);
Skin/soft tissue infections (Staphylococci) Less effective than other PCNs
Use ONLY if bugs make penicillinase (PCN-resistant; MRSA);
Hypersensitivity reaction Elimination=kidneys and BILE;
Vancomycin is DOC for PCN-resistant bugs; NOT for GRAM (-)

Front 30

amoxicillin

Back 30

Aminopenicillin; Extended spectrum Penicillin IRREVERSIBLY binds the active site of transpeptidase; Acid stable (oral) Otitis;
Upper Respiratory Tract infection
(S. pneumoniae and
H. influenza) MOST ACTIVE oral β-lactam against PCN-resistant S. pneumonia;
Hypersensitivity reaction Elimination=kidneys

Front 31

ampicillin

Back 31

Aminopenicillin; Extended spectrum Penicillin; IRREVERSIBLY binds the active site of transpeptidase; ORAL
tx: Meningitis (L. monocytogenes in immunocompro-mised)
NOTE: When caused by S.pneumonieae (like in kids), tx. requires a cocktail. Hypersensitivity reaction Elimination=kidneys and BILE

Given in cocktail with vancomycin and 3rd gen. cephalosporin.

If a rash appears with tx, think MONO.

Front 32

piperacillin

Back 32

Anti-pseudomonal; Extended spectrum Penicillin; IRREVERSIBLY binds the active site of transpeptidase Acid labile (parenteral)
tx: GRAM (-) BUGS, Lyme disease; Nosocomial pneumonia (P.aeruginosa); Bite wounds (often combined w/β-lactamase inhibitor like clavulanate, sulbactam, tazobactam)
Hypersensitivity reaction Elimination=kidneys

Front 33

ticarcillin

Back 33

Extended spectrum Penicillin; IRREVERSIBLY binds the active site of transpeptidase; Acid labile (parenteral)
Hypersensitivity reaction Elimination=kidneys

tx gram - bugs mainly Pseudomonas

Front 34

clavulanate

Back 34

β-lactamase inhibitor Irreversibly bind β-lactamases to inactivate them.
Amoxicillin + clavulanate= augmentin inc effectiveness

Do not mix w/ cephalosporins???
---these agents irrev bind B lactam prod by wide range of bact. Active against plasmid encoded BMS including the extended spectrum BLMs that hydrolyze ceftazidime and ceftaxime (3rd gen.), Inactive against type I chromosomal BLMs induced in Enterobacter, Acinetobacter and Citrobacter by 2nd & 3rd gen. cephalosporins.

Front 35

sulbactam

Back 35

β-lactamase inhibitor Ampicillin + sulbactam
Irreversibly bind β-lactamases to inactivate them. inc effectiveness
Do not mix w/ cephalosporins???
---these agents irrev bind B lactam prod by wide range of bact. Active against plasmid encoded BMS including the extended spectrum BLMs that hydrolyze ceftazidime and ceftaxime (3rd gen.), Inactive against type I chromosomal BLMs induced in Enterobacter, Acinetobacter and Citrobacter by 2nd & 3rd gen. cephalosporins.

Front 36

tazobactam

Back 36

Piperacillin + tazobactam
Irreversibly bind β-lactamases to inactivate them.
Do not mix w/ cephalosporins???
---these agents irrev bind B lactam prod by wide range of bact. Active against plasmid encoded BMS including the extended spectrum BLMs that hydrolyze ceftazidime and ceftaxime (3rd gen.), Inactive against type I chromosomal BLMs induced in Enterobacter, Acinetobacter and Citrobacter by 2nd & 3rd gen. cephalosporins.

Front 37

cephalexin

Back 37

1st Generation Cephalosporin Similar to PCNs; inhibits cell wall synthesis. Oral
tx: Primarily GRAM (+) and some GRAM (-) Skin and soft tissue infections (Streptococci)
Highly resistant to penicillinase; less likely than PCN to cause hypersensitivity;
If mild rxn to PCN, use cephalosporin; If severe rxn to PCN, DO NOT use cephalosporins.
Cross-sensitivity w/PCNs Elimination=kidneys; Dose modification in renal dysfxn.
NO CNS entry;

NOT effective against LAME (Listeria monocytogenes, Atypicals like Chlamydia and mycoplasma, MRSA, Enterococci)

Front 38

cefazolin

Back 38

1st Generation Cephalosporin Similar to PCNs; inhibits cell wall synthesis. Parenteral
tx: Primarily GRAM (+) and some GRAM (-) Serious Streptococci infections; Surgical prophylaxis (Staphylococci and Gram (-) enteric bacilli)
Highly resistant to penicillinase; less likely than PCN to cause hypersensitivity.
If mild rxn to PCN, use cephalosporin;
If severe rxn to PCN, DO NOT use cephalosporins.
Cross-sensitivity w/PCNs
Elimination=kidneys; Dose modification in renal dysfxn.
Preferred among 1st gen. due to longer t ½.
NO CNS entry, NOT effective against LAME pathogens

Front 39

cefotetan

Back 39

2nd gen Less important
intra-abdoinal, gynecologic and biliary tract infections
not effective against lame pathogens; No CNS entry
inhibits cell wall synthesis

Front 40

cefoprozil

Back 40

2nd Generation Cephalosporin Similar to PCNs; inhibits cell wall synthesis. Oral
Gram (+) and increasing activity of Gram (-); Otitis (amoxicillin resistant H. influenza); 2nd choice drug after amoxicillin; (cefuoxime axetil also indicated)
Highly resistant to penicillinase; less likely than PCN to cause hypersensitivity.
If mild rxn to PCN, use cephalosporin;
If severe rxn to PCN, DO NOT use cephalosporins.
Cross-sensitivity w/PCNs Elimination=kidneys; Dose modification in renal dysfxn.
NO CNS entry
NOT effective against LAME pathogens

Front 41

cefuroxine sodium

Back 41

2nd Generation Cephalosporin Similar to PCNs; inhibits cell wall synthesis. Oral or Parenteral
tx: Gram (+) and increasing activity of Gram (-); Emperic therapy for community acquired pneumo.;
Otitis (amoxicillin resistant H. influenza)
Highly resistant to penicillinase; less likely than PCN to cause hypersensitivity.
If mild rxn to PCN, use cephalosporin;
If severe rxn to PCN, DO NOT use cephalosporins.
Cross-sensitivity w/PCNs Elimination=kidneys; Dose modification in renal dysfxn.

ONLY 2nd generation to enter CNS!
NOT effective against LAME pathogens

Front 42

cefoxitin

Back 42

2nd Generation Cephalosporin Similar to PCNs; inhibits cell wall synthesis. Parenteral
tx: Gram (+) and increasing activity of Gram (-); Surgical prophylaxis

Highly resistant to penicillinase; less likely than PCN to cause hypersensitivity.
If mild rxn to PCN, use cephalosporin;
If severe rxn to PCN, DO NOT use cephalosporins.
Cross-sensitivity w/PCNs Elimination=kidneys; Dose modification in renal dysfxn.
NO CNS entry
NOT effective against LAME pathogens

Front 43

ceftazidime

Back 43

3rd Generation Cephalosporin Similar to PCNs; inhibits cell wall synthesis. Parenteral
tx: Broader range (+) and (-); greater activity GRAM (-); Gonorrhea, Urinary tract and intraabdominal infections, Otitis media, Meningitis, Pneumonia, Lyme disease (Enterobacteriacae, H. influenzae, M.catarrhalis) HEN PECKS
Less likely than PCN to cause hypersensitivity. If mild rxn to PCN, use cephalosporin;
If severe rxn to PCN, DO NOT use cephalosporins.
Hydrolyzed by extended spectrum β-lactamases.
Cross-sensitivity w/PCNs Elimination=kidneys; Dose modification in renal dysfxn.
ENTERS CNS
Usually a “best pick”
NOT effective against LAME pathogens

Front 44

cefdinir

Back 44

3rd Generation Cephalosporin Similar to PCNs; inhibits cell wall synthesis. Parenteral
tx: Broader range (+) and (-); greater activity GRAM (-);
Gonorrhea, Urinary tract and intraabdominal infections, Otitis media, Meningitis, Pneumonia, Lyme disease (Enterobacteriacae, H. influenzae, M.catarrhalis)
Less likely than PCN to cause hypersensitivity. If mild rxn to PCN, use cephalosporin;
If severe rxn to PCN, DO NOT use cephalosporins.
Hydrolyzed by extended spectrum β-lactamases.
Cross-sensitivity w/PCNs Elimination=kidneys; Dose modification in renal dysfxn.
ENTERS CNS
Usually a “best pick”
NOT effective against LAME pathogens

Front 45

ceftriaxone

Back 45

3rd Generation Cephalosporin Similar to PCNs; inhibits cell wall synthesis. Parenteral
tx: Broader range (+) and (-); greater activity GRAM (-); Gonorrhea, Urinary tract and intraabdominal infections, Otitis media, Meningitis, Pneumonia, Lyme disease (Enterobacteriacae, H. influenzae, M.catarrhalis)
Highly resistant to penicillinase;
less likely than PCN to cause hypersensitivity.
If mild rxn to PCN, use cephalosporin;
If severe rxn to PCN, DO NOT use cephalosporins.

Cross-sensitivity w/PCNs Elimination=BILE
ENTERS CNS
Usually a “best pick”

NOT effective against LAME pathogens

LIVER PROBLEMS NO BUT RENAL PROBLEMS OKAY

Front 46

cefepime

Back 46

4th Generation Cephalosporin Similar to PCNs; inhibits cell wall synthesis. Parenteral
tx: GRAM (-) BUGS; Nosocomial pathogens (Citrobacter freundii and Enterobacter cloacae)

Targets gram negative VERY resistant to β-lactamases; less likely than PCN to cause hypersensitivity.
If mild rxn to PCN, use cephalosporin;
If severe rxn to PCN, DO NOT use cephalosporins.
Cross-sensitivity w/PCNs Elimination=kidneys; Dose modification in renal dysfxn.

ENTERS CNS
NOT effective against LAME pathogens

Front 47

aztreonam****

Back 47

Monobactam (monocyclic β-lactam) Cell wall synthesis inhibitor Parenteral AEROBIC GRAM (-)
Enterobacter, Citrobacter, Klebsiella, Proteus, P. aeruginosa

NOT for use on GRAM (+) or anaerobic bacteria.

Good for use against mult-drug resistant strains of organisms in therapeutic use column.
Resistant to many β-lactams from gram (-) bugs
Hypersensitivity; thrombophlebitis Use in patients allergic to PCNs and cephalosporins.*****

Front 48

imipenem

Back 48

Carbapenem Cell wall synthesis inhibitor; preferentially binds PBP-2 Parenteral
tx: Gram (+) and Gram (-) including many aerobic and anaerobic gram (-) bacilli; Systemic infections
Esp mixed infections caused by aerobic and anaerobic enteric bacilli
Cross-sensitivity with PCNs, cephalosporins, and other β-Lactams….AVOID in allergic pts.

Seizures in pts w/epilepsy; anemia, thrombocytopenia Elimination=kidneys
Inactivated by renal dehydropeptidase, so enzyme inhibitor (CILASTIN) given in conjuction.
PROBENACID inhibits renal excretion.

Front 49

meropenem

Back 49

Carbapenem Cell wall synthesis inhibitor; Preferentially binds PBP-3 Parenteral Gram (+) and particularly Gram (-) including many aerobic and anaerobic gram (-) bacilli;
Systemic infections
Esp mixed infections caused by aerobic and anaerobic enteric bacilli Cross-sensitivity with PCNs, cephalosporins, and other β-Lactams….AVOID in allergic pts.

Seizures in pts w/epilepsy; anemia, thrombocytopenia Elimination=kidneys
PROBENACID inhibits renal excretion.

Front 50

vancomycin

Back 50

“Other”
Cell wall synthesis inhibitor Oral or parenteral
tx: Gram (+) cocci and bacilli
Serious infections caused by PCN-resistant organisms (MRSA, enterococci)
Can be toxic-red man syndrome; erythematous rash on face/upper body Elimination=Kidneys Poorly absorbed from the gut
Used if diclocillin and nafcillin don’t work

Front 51

bacitracin

Back 51

“Other”
Cell wall synthesis inhibitor Topical
tx: Minor skin and ocular infections (Staphylococci and Streptococci) Gram (+) Nephrotoxicity Sold in OTC ointments

Front 52

fosfomycin

Back 52

“Other”
Cell wall synthesis inhibitor
Oral
tx: Uncomplicated UTI ; Diarrhea

Single oral dose which is excreted unchanged in the urine and feces irrev inhibits enolpyruvyl transferase in the initial stages of cell wall peptidoglycan synthesis

Front 53

amikacin

Back 53

Aminoglycoside; bacteriocidal
Inhibitor protein synthesis via 30S ribosomal subunit; LOCKS the 2 subunits in place at the start codon = causes misreading of mRNA so premature termination of translation or incorporation of incorrect amino acids.
Parenteral
tx: Aerobic Gram (-) Bacilli;
Used when infection is resistant to other aminoglycosides.
resistant to enzyme inact
Adjust dosing based on creatinine clearance levels;
Blocked by low pH.
Resistant to acetylase, adenylase and phosphorylase.
NEPHROTOXIC: Accumulates in prox. tubules resulting in acute necrosis.
OTOTOXIC: Accumulation in labyrinth and hair cells of cochlea.
Elimination=kidneys
Long post-antibiotic effect.
Does not enter CNS or host cells.
Poorly absorbed.
“A = aerobic”

Front 54

gentamicin

Back 54

Aminoglycoside; bacteriocidal
Inhibitor protein synthesis via 30S ribosomal subunit; LOCKS the 2 subunits in place at the start codon = causes misreading of mRNA so premature termination of translation or incorporation of incorrect amino acids.
Parenteral or Topical
tx: Aerobic Gram (-) Bacilli; Most active against Enterobacteriaceae species.
Adjust dosing based on creatinine clearance levels;
Blocked by low pH.
Inactivated by acetylase, adenylase and phosphorylase.
NEPHROTOXIC: Accumulates in prox. tubules resulting in acute necrosis.
OTOTOXIC: Accumulation in labyrinth and hair cells of cochlea.
Elimination=kidneys
Long post-antibiotic effect.
Does not enter CNS or host cells.
Poorly absorbed.
“A = aerobic”

Front 55

neomycin

Back 55

Aminoglycoside; bacteriocidal
Inhibitor protein synthesis via 30S ribosomal subunit; LOCKS the 2 subunits in place at the start codon = causes misreading of mRNA so premature termination of translation or incorporation of incorrect amino acids.
TOPICAL only most nephrotoxic
tx: Aerobic Gram (-) Bacilli;
Limited to TOPICAL treatments.
Adjust dosing based on creatinine clearance levels; Blocked by low pH. Inactivated by acetylase, adenylase and phosphorylase.
NEPHROTOXIC: Accumulates in prox. tubules resulting in acute necrosis. OTOTOXIC: accumulation in labyrinth and hair cells of cochlea.
Elimination=kidneys
Long post-antibiotic effect.
Does not enter CNS or host cells.
“A = aerobic”

Front 56

streptomycin

Back 56

Aminoglycoside; bacteriocidal
Inhibitor protein synthesis via 30S ribosomal subunit; LOCKS the 2 subunits in place at the start codon = causes misreading of mRNA so premature termination of translation or incorporation of incorrect amino acids.
IM
tx: Aerobic Gram (-) Bacilli;
Least active against Pseudomonas aeruginosa; Multi-drug resistant tuberculosis, plague (Yersinia pestis), and tularemia (Francisella tularensis); “RABBIT HUNTERS”
Adjust dosing based on creatinine clearance levels; Blocked by low pH. Inactivated by acetylase, adenylase and phosphorylase.
NEPHROTOXIC: Accumulates in prox. tubules resulting in acute necrosis. OTOTOXIC: Accumulation in labyrinth and hair cells of cochlea.
Elimination=kidneys
Long post-antibiotic effect.
Does not enter CNS or host cells.
Poorly absorbed.
LEAST toxic of the aminoglycosides
“A = aerobic”

Front 57

tobramycin

Back 57

Aminoglycoside; bacteriocidal
Inhibitor protein synthesis via 30S ribosomal subunit; LOCKS the 2 subunits in place at the start codon = causes misreading of mRNA so premature termination of translation or incorporation of incorrect amino acids.
Parenteral or topical
tx: Aerobic Gram (-) Bacilli;
Most active against PSEUDOMONUS aeruginosa
Adjust dosing based on creatinine clearance levels; Blocked by low pH. Inactivated by acetylase, adenylase and phosphorylase.
NEPHROTOXIC: Accumulates in prox. tubules resulting in acute necrosis. OTOTOXIC: Accumulation in labyrinth and hair cells of cochlea. Elimination=kidneys
Long post-antibiotic effect.
Does not enter CNS or host cells.
Poorly absorbed.
“A = aerobic”

Front 58

tetracycline

Back 58

Tetracycline; bacteriostatic
Inhibitor of protein synthesis via 30S ribosomal subunit; PhYSICALLY BINDS to prevent access of aminoacyl-tRNA to the A site.
Parenteral or oral
tx: Broad spectrum; DOC for Rocky Mtn. Spotted fever (Rickettsia) and Lyme Disease.
Also, Peptic ulcers (H.pylori) Bioavailability is reduced in certain foods (binds divalent cations…Ca, Al and Fe and is deactivated)
DO NOT take w/antacids or Iron supplements, dairy products, etc.
Discoloration of teeth;
Photosensitivity (absorbs UV and looks like sunburn)
Nephrotoxicity; Hepatotoxicity Elimination=kidneys and bile
“T = ticks”

Front 59

doxycycline

Back 59

Tetracycline; bacteriostatic
Inhibitor of protein synthesis via 30S ribosomal subunit; PhYSICALLY BINDS to prevent access of aminoacyl-tRNA to the A site.
Parenteral or oral
Broad spectrum; DOC for Rocky Mtn. Spotted fever (Rickettsia) and Lyme Disease. Also, Genital infections (Chlamydia) Bioavailability is reduced in certain foods (binds divalent cations…Ca, Al and Fe and is deactivated)
DO NOT take w/antacids or Iron supplements, dairy products, etc.
Discoloration of teeth;
Photosensitivity (absorbs UV and looks like sunburn)
Nephrotoxicity; Hepatotoxicity Elimination=kidneys and bile
NOTE: NOT DEPT ON RENAL EXCRETION!!! (USE in pts with renal dysfxn.)
“T = ticks”

Front 60

minocycline

Back 60

Tetracycline; bacteriostatic
Inhibitor of protein synthesis via 30S ribosomal subunit; PYSICALLY BINDS to prevent access of aminoacyl-tRNA to the A site. Parenteral or oral
Broad spectrum; DOC for Rocky Mtn. Spotted fever (Rickettsia) and Lyme Disease.
Also, acne vulgaris
Effective in CNS and penetrates skin well. Bioavailability is reduced in certain foods (binds divalent cations…Ca, Al and Fe and is deactivated)
DO NOT take w/antacids or Iron supplements, dairy products, etc.
Discoloration of teeth;
Photosensitivity (absorbs UV and looks like sunburn)
Nephrotoxicity; Hepatotoxicity Elimination=kidneys and bile
“T = ticks”

Front 61

what do the inhibitors of protein synthesis do?

Back 61

These agents selectively disrupt bacterial protein synthesis; Differences in bacterial ribosome structure; Differences in bacterial ribosome function
either 30s or 50s
do not directly alter enzyme instead bind to 30 or 50 to prevent appropriate interaction
prevent translocation from A to P site prevents tRNA binding to ribosome

Front 62

are tetracyclines bacteriocidal or static?

Back 62

bacteriostatic

Front 63

are aminoglycosides bacteriocidal or static?

Back 63

bacteriocidal

Front 64

what are the 30S ribosombal binding drugs?

Back 64

aminoglycosides and tetracyclines

Front 65

what are the 50s ribosomal binding drugs?

Back 65

chloramphenicol, clindamycin, macrolides, mupirocin, streptogramins

CCMMS

Front 66

name the protein synthesis inhibitors

Back 66

aminoglycosides, cholormaphenicol, clindamycin, macrolides, mupirocin, streptogramins, tetracyclines

Front 67

describe aminoglycosidal function

Back 67

glycosidic bond, poorly absorbed in gut, postantibiotic effect, elim in kidneys NOT met in liver;
do not cross CNS

Front 68

adverse effects of aminoglycosides

Back 68

nephrotoxic-prox tubules necrosis
ototoxic

Front 69

tetracycline function

Back 69

bind 30s, prevent tRNA access to A site, bacteriostatic; broad spec; high oral availability unless taken w/ metals or antacids, iron, dairy

Front 70

side effects of tetracyclines

Back 70

discoloration of teeth, photosn (accum under skin and absorbs UV), nephrotoxicity and hepatotoxicity

Front 71

tetracycline that is not dependent on renal

Back 71

doxycylcine

Front 72

tetracycline that can penetrate the CNS and skin

Back 72

minocycline

Front 73

If someone is immunocomprimised what does the drug need to be?

Back 73

bacteriocidal

Front 74

do not take tetracyclines w/ what?

Back 74

trace metals Fe, Ca, Al
antacids, dairy ect

Front 75

Which of the following is indicated for treatment of bacterial meningitis in a 2 yr-old boy caused by H. influenzae? Cefotaxime
Cefoxitin , Cefprozil , Penicillin G, Vancomycin

Back 75

cefotaxime---3rd gen can cross CNS effective against gram neg

Front 76

An adult female presents with a urinary tract infection caused by an aerobic gram-negative bacillus. She has previously had a hypersensitivity reaction to penicillin G. Which of these agents is indicated? Cefazolin, Clavulanic acid, Imipenem, Aztreonam
Amoxicillin

Back 76

aztreonam---gen safe when allergic to PCNs and cephalosporins

Front 77

Which of the following parenteraly administered agents would be most effective against β-lactamase producing strains of H. influenzae and N. gonorrhoeae? Amoxicillin, Cefdinir, Ceftriaxone, Piperacillin, Penicillin G

Back 77

ceftiaxone---parenteral
vs
cefdinir--oral

the others are sensitive to B lactamasesl

Front 78

Which of the following agents is most active against Pseudomonas aeruginosa? Ampicillin, Penicillin G, Penicillin V, Nafcillin, Piperacillin

Back 78

piperacillin

Front 79

An adult female is admitted to the hospital with endocarditis caused by a penicillinase-producing Staphylococcus aureus infection and requires parenteral therapy. Which of the following agents is indicated? Ampicillin, Amoxicillin , Dicloxacillin, Nafcillin, Penicillin G

Back 79

nafcillin---parenteral
other choice but oral is dicloxacillin

Front 80

cefotaxime

Back 80

3rd gen cephalosporin; sim to PCNs; inhibits cell wall synthesis
parenteral
broader rang + and - greater activity gram -
gonorrhea, UTI and intraabdominal infections, otitis media, meningitis, pneumonia, lyme disease (enterobacteriacae, HI, m catarrhalis)
less like to cause HS, mild rxn use if severe rxn to PCN do NOT use
hydrolyzed by extended spec B-lactams
cross sn w/ PCNs
elim=kidnes; dose mod in renal dysfxn
ENTERS CNS-->treats meningitis
usually best pick out of cephs
not effective against LAME pathogens

Front 81

cefdinir

Back 81

MUST BE GIVEN ORALLY
WOULD BE EFFECTIVE AGAINST GRAM -

3rd gen cephalosporin; sim to PCNs; inhibits cell wall synthesis
parenteral
broader rang + and - greater activity gram -
gonorrhea, UTI and intraabdominal infections, otitis media, meningitis, pneumonia, lyme disease (enterobacteriacae, HI, m catarrhalis)
less like to cause HS, mild rxn use if severe rxn to PCN do NOT use
hydrolyzed by extended spec B-lactams
cross sn w/ PCNs
elim=kidnes; dose mod in renal dysfxn
ENTERS CNS-->treats meningitis
usually best pick out of cephs
not effective against LAME pathogens

Front 82

what are b lactamases

Back 82

kill penicillins they are enzymes against them even destroy extended specrum like amoxicillin

penicillinase is a specific B lactamase

use clavulonate, sulbactam and lazobactam to be a BLI!!!

Front 83

Drugs that affect the 50S Ribosomal Subunit

Back 83

Drugs that affect the 50S Ribosomal Subunit--Macrolides , Ketolides , Chloramphenicol , Clindamycin , Quinupristin-Dalfopristin
Linezolid

Front 84

macrolides

Back 84

50S ribosomal subunit and prevent TRANSLOCATION of the nascent peptide from the A site (aminoacyl site) to the P site (peptidyl site). This blockade inhibits binding of the next aminoacyl tRNA to the ribosome.
ORAL
Absorption and activity of erythromycin is reduced by gastric acid.
--Azythromycin and clarithromycin are more readily absorbed, have a longer t1/2 and achieve higher tissue concentrations. These two drugs are less likely to cause GI distress
Excretion-Bile and urine;

Front 85

azithromycin

Back 85

Macrolide Inhibitor of protein synthesis via 50S ribosomal subunit; prevents translocation of nascent peptide from A to P site. Incoming tRNA can’t bind.
Oral
URTi and pneumonia, esp: Chlamydia, H. influenza, *otitis media, *sinusitis; M. pneumonia
L. pneumonia; Generally for all macrolides: Streptococci
Pneumococci; BORDATELLA DOC!!!!
Little effect on CYP3A4 Elimination=Kidney and bile;
More readily absorbed, longer ½ life, higher tissue concentrations.

**less GI distress DOC if P450 drug intx

Front 86

clarithromycin

Back 86

Macrolide
Inhibitor of protein synthesis via 50S ribosomal subunit; prevents translocation of nascent peptide from A to P site. Incoming tRNA can’t bind.
Oral
URTi and pneumonia, esp:
****DOC H. pylori ; Generally for all macrolides: Streptococci, Pneumococci
CYP3A4 inhibition = possible toxicity of other drugs (esp. statins) Elimination=Kidney and bile;
****More readily absorbed, longer ½ life, higher tissue concentrations.

Front 87

erythromycin

Back 87

Macrolide Inhibitor of protein synthesis via 50S ribosomal subunit; prevents translocation of nascent peptide from A to P site. Incoming tRNA can’t bind.
Oral
URTi and pneumonia:
neonatal chalmydia eye drops, DOC legionella
Streptococci, Pneumococci Absorption reduced by gastric acid = gastric distress;
CYP3A4 inhibition = possible toxicity of other drugs (esp. statins)
Elimination=Kidney and bile

Front 88

telithromycin

Back 88

Ketolide
Similar to macrolides; 2 separate binding sites on 50S subunit.
Oral w/o regard to food
Acute sinusitis, acute exacerbations of chronic bronchitis by S. pneumonia and H. influenza
Adverse effects: Nausea, diarrhea, prolonged Q/T interval, impairs visual accomodation
CONTRAINDICATION: don’t take with antiarrythmics

More stable to stomach acid; don’t have to take w/food. Long ½ life (10 h); Less susceptible to bacterial export pumps.

METHYLASE DOES NOT INACTIVATE!!!

Front 89

which macrolide has reduced absorption?

Back 89

erythromycin

Front 90

which 2 macrolides have CYP3A4 inhibition?

Back 90

clarithromycin and erythromycin

Front 91

route of preparation for macrolides

Back 91

oral

Front 92

clindamycin

Back 92

Inhibitor of protein synthesis via 50S ribosomal subunit by binding peptidyltransferase site and preventing transpeptidation; incoming tRNA can’t bind (same as macrolide) Parenteral,
Topical or Oral
Penicillin-resistant Streptococci
Anaerobic bacteria:
Bacteriodes fragilis
Clostridium perfringens High risk of GI SUPERINFECTION (Clostridium dificile growth enhanced…fatal diarrhea) – stop tx and give metronidazole or vancomycin
Pseudomembranous colitis Elimination=kidney and bile

DOES not enter CNS

Front 93

chloramphenicol

Back 93

Inhibitor of protein synthesis via 50S ribosomal subunit (MOA same as clindamycin) Parenteral,
Topical or Oral
Broad spectrum of meningitis:
Pneumococci
Meningococci
H. influenzae Neonates deficient in glucuronosyl-transferase so DECREASE dosage;
Anemia d/t inhibition of iron incorporation into heme.
Gray baby syndrome Elimination=kidney (after glucuronate conjugation)
Enters CNS

Front 94

quinupristin-dalfopristin

Back 94

Streptogramin Inhibitor of protein synthesis via 50S ribosomal subunit.
Synergistic effect: Q inhibits synthesis of tRNA (prevention of add’n to new peptide chain), and D inhibits peptidyl transferase (blocks formation of peptide bond). Parenteral NASTY BUGS (but not CNS)
Vancomycin-resistant organisms or if pt. has red-man syndrome. Inflammation of veins;
Arthralgia;
Myalgia;
Diarrhea

Think “vancomycin-resistant”

Front 95

linezolid

Back 95

Oxazolidine-diones Inhibitor of protein synthesis by binding the 23S ribosomal RNA of the 50S ribosomal subunit. (Prevents formation of 70S initiation complex) Parenteral or oral NASTY BUGS
Aerobic Gram (+):
Vancomycin-resistant E. faecium
MRSA Cross-resistance with other drugs unlikely due to unique MOA. Oral bioavailability is 100%; 30% excreted in urine unchanged.

Front 96

mupirocin

Back 96

Inhibitor of protein synthesis via 50S ribosomal subunit. Side chain mimics isoleucine so competes for isoleucine tRNA synthetase. Topical Most Staphylococci
First effective topical tx. for impetigo (staphylococci or streptococci) Cross-resistance with other drugs unlikely due to unique MOA.

Front 97

what infection can clindamycin CAUSE?

Back 97

C. diff

Front 98

what metabolizes chloramphenicol?

Back 98

glucuronosyl-transferase

Front 99

what treats vancomycin-resistant organisms?

Back 99

quinupristin dalfopristin

Front 100

topical drug for staph and strep?

Back 100

mupirocin

Front 101

. inactivation of aminoglycosides by

Back 101

by acetylase, adenylase and phosphorylases,

Front 102

sulfamethoxazole

Back 102

Sulfonamide Antifolate: Block dihydropteroate synthase (first step in folate metabolism):
Pteridine + PABA -->Dihydro-folic acid
Oral
tx: Urinary tract infections Inactivated by N-acetylation; can precipitate in renal tubules causing crystalluria (Sufficient hydration is mandatory)
***Rash; erythema multiforme; Steven-Johnson syndrome; hemolytic anemia in G6PD deficiency. ½ life is 11 hours

THINK “UTI and Kidney”
rapidly absorbed

Front 103

silver sulfadiazine

Back 103

Sulfonamide
Antifolate: Block dihydropteroate synthase (first step in folate metabolism):
Pteridine + PABA --> Dihydro- folic acid
Topical
Prevention of infection from burns
Inactivated by N-acetylation; can precipitate in renal tubules causing crystalluria (Sufficient hydration is mandatory)
***Rash; erythema multiforme; Steven-Johnson syndrome; hemolytic anemia in G6PD deficiency.

Front 104

sulfacetamide

Back 104

Sulfonamide
Antifolate: Block dihydropteroate synthase (first step in folate metabolism):
Pteridine + PABA -->Dihydro- folic acid
Topical
Ocular infections (pink eye) Inactivated by N-acetylation; can precipitate in renal tubules causing crystalluria (Sufficient hydration is mandatory)
***Rash; erythema multiforme; Steven-Johnson syndrome; hemolytic anemia in G6PD deficiency.

Front 105

trimethoprim

Back 105

Antifolate: Binds bacterial folate reductase to prevent:Dihydrofolic acid --> Tetrahy-drofolic acid
Oral
Bacterial prostatitis, Vaginitis Hematologic disorders; Rash;
Nausea
A synthetic, aminopyrimidine drug;
Weak base, concentrates in acidic tissues.
blocks 100K times more than mammalian

Front 106

TMP-SMX

Back 106

Antifolate;
combination drug--synergistic
Parenteral or oral
Urinary tract infections and prostate infections:E. coli, K. pneumonia, Proteus species, Enterobacter species; DOC for pulmonary infections (Pneumocystis jirovecii** and Nocardia asteroids) typ. in immune-compromised pt.
NOT active against Psuedomonas aeruginosa which is often the cause of UTIs in hospitalized pts.

Front 107

name 2 antifolate drugs

Back 107

SMX and TMP

Front 108

name the fluoroquinolones

Back 108

ciprofloxacin and levofloxacin

Front 109

describe folate synthesis in bacteria and how it is blocked

Back 109

SMX--Folate synthesis in bacteria is initiated with the fusion of pteridine and (PABA) to form dihydrofolate.

TMP-prevents bacterial folate reductase ; Dihydrofolic acid --> Tetrahy-drofolic acid

Front 110

fluoroquinolones describe their aborption and distribution

Back 110

well absorbed and widely distributed, More concentrated in many tissues compared to plasma, Lungs, kidneys, prostate, endometrium and ovaries; Long postantibiotic effect-Bactericidal, Concentration-dependent killing, Chelate divalent and trivalent cations, Inhibit the metabolism of caffeine, Reduce caffeine intake to reduce CNS stimulation

Front 111

fluroquinolones and rxns to other molecules

Back 111

Chelate divalent and trivalent cations, Inhibit the metabolism of caffeine, Reduce caffeine intake to reduce CNS stimulation

Front 112

MOA of fluoroquinolones

Back 112

Inhibits bacterial DNA topoisomerase, type II (DNA gyrase), Induce negative supercoils in the circular DNA which eliminate the positive supercoils present ahead of the DNA replication fork
type IV -Separates the DNA once replication is complete (decatenation), these enzymes maintain DNA in a stable and biologically active form; DNA gyrase targeted in gram – bacteria and type 4 is inhibited in gram + bacteria

Front 113

ciprofloxacin

Back 113

Fluoroquino-lone Inhibits bacterial DNA topoisomerase: Gram (-): Type II DNA gyrase (normally adds in negative supercoils to smooth out DNA at replication fork). Gram (+): Type IV (normally separates DNA once replication is complete) .
Parenteral, Topical, or Oral
tx: GRAM (-) bacteria (less effective against gram (+)
Urinary tract inf. Enterobacteriaceae and P. aeruginosa), Bacterial diarrhea (Campylobacter, Salmonella, E.coli)

Chelates divalent cations (avoid dairy products). Inhibits metabolism of caffeine (reduce caffeine intake).
Children: arthropathy and osteochondrosis Well absorbed and concentrate in lungs, kidneys, prostate, endometrium and ovaries.
Long postantibiotic effect.

Front 114

levofloxacin

Back 114

Fluoroquino-lone Inhibits bacterial DNA topoisomerase: Gram (-): Type II DNA gyrase (normally adds in negative supercoils to smooth out DNA at replication fork). Gram (+): Type IV (normally separates DNA once replication is complete)
Parenteral or oral
Urinary tract inf.Enterobacteriaceae and P. aeruginosa). Bacterial diarrhea (Campylobacter, Salmonella, E.coli). Resp. tract inf. (Pneumococi, H. influenzae and
M. catarrhalis). Ocular infections

Chelates divalent cations (avoid dairy products). Inhibits metabolism of caffeine (reduce caffeine intake).
Children: arthropathy and osteochondrosis
Well absorbed and concentrate in lungs, kidneys, prostate, endometrium and ovaries.
Long postantibiotic effect.
THINK “pneumonia”

Front 115

moxifloxacin

Back 115

Fluoroquino-lone Inhibits bacterial DNA topoisomerase: Gram (-): Type II DNA gyrase (normally adds in negative supercoils to smooth out DNA at replication fork). Gram (+): Type IV (normally separates DNA once replication is complete)
Oral
Inc’d activity against pneumococci;
Urinary tract inf. (Enterobacteriaceae and P. aeruginosa). Bacterial diarrhea (Campylobacter, Salmonella, E.coli)
Resp. tract inf. (Pneumococi,
H. influenzae and M. catarrhalis)
Ocular infections.
Chelates divalent cations (avoid dairy products). Inhibits metabolism of caffeine (reduce caffeine intake).
Children: arthropathy and osteochondrosis Well absorbed and concentrate in lungs, kidneys, prostate, endometrium and ovaries.
Long postantibiotic effect.
THINK “pneumonia”

Front 116

norfloxacin

Back 116

Fluoroquino-lone Inhibits bacterial DNA topoisomerase: Gram (-): Type II DNA gyrase (normally adds in negative supercoils to smooth out DNA at replication fork). Gram (+): Type IV (normally separates DNA once replication is complete)
Oral
Urinary tract infection (Enterobacteriaceae and P.aeruginosa)
Chelates divalent cations (avoid dairy products). Inhibits metabolism of caffeine (reduce caffeine intake).
Children: arthropathy and osteochondrosis ONLY for UTI due to rapid rate of excretion.

Front 117

nitrofurantoin

Back 117

Bacterial enzymes reduce this to highly active metabolites that damage bacterial DNA nearby. Oral UTI; particularly acute infections in urinary bladder (E.coli and enterococci) Turns urine brown
Acidic urine (pH<5) increases activity to damaging metabolites.
RESISTANT: Proteus, Psuedomonas, Enterobacter and Klebsiella
(so NOT for use in hospital acquired infections)
GI irritation Rapid elimination = kidneys

Front 118

daptomycin

Back 118

Disrupts plasma membrane fxn w/o entering the cytoplasm. Topical Drug resistant
GRAM (+) skin infections: MRSA, vancomycin-resistant S.aureus, and vancomycin-resistant enterococci -- Unique lipoprptide antibiotic

THINK “skin infection”

Front 119

polymyxin B

Back 119

Interacts w/phospholipid part of bacterial cell to disrupt mb integrity Topical GRAM (-) bacilli Ineffective on Proteus species.
Nephrotoxicity

Front 120

rifaximin

Back 120

Inhibits bacterial RNA synthesis; inhibits DNA-dependent RNA polymerase Oral Traveler’s diarrhea (E.coli non-invasive strains) Non-absorbed so readily moves to intestines @ site of action. THINK “traveler’s diarrhea”

Front 121

An adult female presents with a urinary tract infection caused by Enterococcus faecalis. Initial therapy with vancomycin is highly ineffective. Which of the following is indicated? Ciprofloxacin, Daptomycin, Nitrofurantoin, Polymyxin B, Rifaximin

Back 121

nitrofurantoin-very effective against vancomycin resistant E. Faecalis

Front 122

Which of the following is most likely to causes cough, dyspnea, pulmonary infiltrates, neutorpenia and paresthsias? Amoxicillin, azithromycin, ciprofloxacin, defepine, nitrofurantoin?

Back 122

used to treat UTI, GI side effects are MC but pulmonary, hematologic and neuropathies are also

nitrofurantoin

Front 123

Crystalluria (precipitation in an acid urine) is most likely to occur after taking which drug without adequate fluids? amoxicillin
Doxycycline, sulfamethoxazole, cephalexin, erythromycin

Back 123

sulfamethoxazole

Front 124

mycobacterial infections describe and name

Back 124

Obligate aerobes, Thrive in oxygen rich tissues (i.e., lung); Intracellular pathogens-macrophage, Hydrophobic with high lipid (mycolic acid) content in the cell wall, Tuberculosis-Mycobacterium tuberculosis( risk of infection is particularly high in immunocomprimised pt); Atypical -mycobacterial infections, Mycobacterium kansasii, Mycobacterium avium-intracellular complex (MAC) –prophylaxis in AIDS pts; Leprosy-Mycobacterium leprae

Front 125

isoniazid

Back 125

Nicotinic acid derivative, Oral preparation, widely distributed following absorption, Extensively metabolized, Key metabolizing enzyme is acetyltransferase (japanese fast, middle eastern slow, US-50/50), Rate of activity is genetically determined
Antimycobacterial Activity-M. tuberculosis-Newly diagnosed (isoniazid will be included in treatment), Exposed neonates or children (isoniazid alone, 3 mo), Latent tuberculosis in TST positive patients that meet one of the following criteria: (isoniazid alone, 9 mo)
HIV+, Chest x-ray indicates non-progressive tuberculosis, IV drug user, Diabetes, Immunocompromised; Active TB: Isoniazid, rifampin, ethambutol and pyrazinamide (with PZA therapy can be reduced to 6 months); INH is effective against some strains of M kansaii NOT MAI or M leprae
Mechanism of Action-Inhibits synthesis of mycolic acid , Mycobacterial cell wall component, Isoniazid is activated by mycobacterial catalase-peroxide (encoded by the katG gene), An isoniazid-enzyme complex is formed which subsequently inhibits enoyl reductase
Enoyl reductase is instrumental in mycolic acid synthesis; Resistance-Mutation in katG; Adverse effects-Hepatitis (risk increases with age), Monitor serum transaminase levels ; Peripheral neuritis-Parathesias Numbness in fingers and toes, Due to drug induced inactivation of vitamin B6 (pyridoxine), Prevent with vitamin supplements

Front 126

what does the mutation in isonizid do?

Back 126

kat G inhibits catalyase to prevent activation so can't inhibit enoyl reductase

Front 127

key metablizing enzyme in isoniazid

Back 127

acetyltransferase

Front 128

what are some side effects of isoniazid?

Back 128

hepatitis, peripheral neuritis (vit B6), hemolysis in G6PD

Front 129

isoniazid

Back 129

First line anitmycobacterial for TB Inhibits synthesis of mycolic acid (cell wall component); Activated by mycobacterial catalase-peroxide forming a complex that inhibits enoyl reductase. Oral M. tuberculosis
-Newly diagnosed
-Exposed neonates or kids (prophylaxis)
-Latent TB in tuberculin skin test (+) pt w/one of the following:
HIV, (+) chest xray, IV drug user, DM, immunocompromised.
Some M. kansasii
KEY: CHRONIC ds; reqs extended tx. Resistance: mutation in katG gene (encodes catalse-peroxide)

Hepatitis (risk increases w/age)
Peripheral neuritis (paresthesias, numbness due to inactivation of Vit. B6

Given as the essential ingredient of a COCKTAIL. Nicotinic acid derivative

Key metabolizing enzyme: acetyltransferase
(Note: rate is genetically determined)

NOT M. avian-int OR M. leprae

9 mo-1 drug for prophylaxis; B6 prevents neuropathy; fast acetylator clears faster
hemolysis in G6PD

Front 130

ethambutol

Back 130

First line anitmycobacterial for TB Two targets: Inhibits RNA synthesis and arabinosyl transferase (necessary for cell wall synthesis) Oral Tuberculous meningitis
(M. tuberculosis and M.avium-intracellulare Optic neuritis;
Impaired red/green discrimination  CONTRAINDICATED in kids <5;
Gout
Thrombocytopenia
Used as a COCKTAIL. Butanol derivative
CNS penetration
80% absorbed in the gut; 75% of that excreted unchanged in urine;
Doesn’t req. activation

Front 131

pyrazinamide

Back 131

First line anitmycobacterial for TB Converted to pyrazinoic acid (the active form) by pyrazinamidase, reducing the pH. (Disrupts mb. energetics and transport fxns.) Oral Tx of M. tuberculosis Gout
Hematologic toxicity
Hepatitis
Elevated Serum Iron
Myalgia, phototoxicity, rash
COCKTAIL w/other first line drugs Nicotinamide derivative
CNS penetration

THINK: “P=pH”

Front 132

rifampin

Back 132

First line anitmycobacterial for TB Active metabolite is deacetylrifampin; Binds DNA-dependent RNA polymerase. Result is inhibition of DNA transcription. Oral Broad spectrum; ALL 4!
M. tuberculosis, M.avium-intercellulare, M.kansasii, and M.leprae Hepatotoxicity, flu-like illness, red-orange discoloration of fluids.
Resistance d/t dec’d affinity of enzyme for drug;
COCKTAIL w/other first line drugs;
Significant drug interactions d/t inducing hepatic enzymes (Ex. OC, anti-HIV drugs, digoxin, halothane, corticosteroids, propanalol, oral anticoagulants.) Elimination = kidney and bile.
Significant enterohepatic recycling Converted to active metabolite in the liver.
Crosses BBB

THINK: “R=RNA polymerase”
INDUCES P450

Front 133

name the combo treatment for TB

Back 133

Isoniazid, rifampin, ethambutol and pyrazinamide (with PZA therapy can be reduced to 6 months)

Front 134

MOA of isonizid

Back 134

inhibits mycolic acid but needs to be activated by catalyse
enoyl reductase assists w/ forming complex

Front 135

adverse effects of isoniazid

Back 135

Hepatitis (risk increases with age), Monitor serum transaminase levels ; Peripheral neuritis-Parathesias Numbness in fingers and toes, Due to drug induced inactivation of vitamin B6 (pyridoxine), Prevent with vitamin supplements

Front 136

ethambutol treats vs isonizid?

Back 136

tuberculous meningitis (M Tb, and MAC) vs TB and some M. kansasaii

Front 137

drug that induces P450

Back 137

rifampin

Front 138

bacteria that rifampin treats

Back 138

all 4!!! M tb, MAC, m kansaii, and M leprae

Front 139

rifabutin

Back 139

Second line anitmycobacterial for TB Similar to Rifampin; Inhibits DNA-dependent RNA polymerase -- Tx of TB in HIV-positive or immunosuppressed pts.

Front 140

cycloserine

Back 140

Second line anitmycobacterial for TB Inhibits cell wall synthesis

Front 141

capreomycin

Back 141

Second line anitmycobacterial for TB Peptide that disrupts protein synthesis  abnormal protein products alter mycobacterial cell wall fxn. Parenteral -- Nephrotoxicity
Ototoxicity
Requires close monitoring

Front 142

ethionamide

Back 142

Second line anitmycobacterial for TB Inhibits acetylation of isoniazid
-- Enhance isoniazid fxn. -- Isoniazid analog

Front 143

dapsone

Back 143

Inhibits folic acid synthesis (similar to sulfonamides) -- Tx of Leprosy (M.leprae) Used in COCKTAIL with RIFAMPIN;
Hemolytic anemia common in G6PD deficient pt.

Front 144

clofazimine

Back 144

Preferentially binds mycobacterial DNA, disrupts DNA replication

Slowly bactericidal to M. leprae
Anti-inflammatory properties prevent erythema nodosum leprosum (a Type II H.S. rxn) GI irritation
Photosensitivity, Skin discoloration
Hepatitis Elimination=feces (unchanged)
Does NOT enter CNS
Very LONG ½ life: 70 days

Front 145

combo treatment for MAC

Back 145

Azithromycin (or Clarithro-mycin) + ethambutol + rifabutin

Front 146

combo prophylaxis for MAC

Back 146

Azithromycin (weekly) or Clarithromycin daily

Front 147

name the 2nd line TB drugs

Back 147

rifabutin, cycloserine, capreomycin, ethionamide,
FLUORQUINOLONES

Front 148

Aminosalicylic acid

Back 148

Inhibits folate biosynthesis by competitively inhibiting p-aminobenzoic acid (PABA)
Poorly tolerated, infrequently used

Front 149

with rifampin or isoniazid resistance in TB what replaces them?

Back 149

fluoroquinolone

Front 150

Enterococcus
Gram + aerobic
Cocci

Back 150

UTI, endocarditis, meningitis

Front 151

Meningococcemia

Back 151

cefotaxime, ceftriaxone

Front 152

Erysipelas

Back 152

Streptococcus pyogenes—penicillin G, amoxicililn

Front 153

Otitis media

Back 153

amoxicillin, cefuroxime sodium (parenteral)

ceprozil is 2nd in line to amoxicillin

Front 154

Impetigo

Back 154

staph infection; cephalexin, dicloxacillin, mupirocin streptococcal, amoxicillin, mupirocin

Front 155

Scarlet fever

Back 155

Strep; Streptococcus—penicillin G, amoxillin

Front 156

Staphylococcus aureus
Gram + aerobic
Cocci

Back 156

skin, soft tissue, RTI, bone; osteomyelitis endocarditis, skin soft tissue infecitons
penicillindiclocillin (if PCN resistant)vancomycinqunupristin-dalfopristin OR daptomycin
Ceph 1-3rd gen cefadroxil,cefazolin, cephalexin, dicloacillin (oral), nafcillin (parenteral) ; vanco if MRSA
linezolid

Front 157

Streptococcus pneumonia
Gram + aerobic
Cocci

Back 157

RTI
Mostly penicillin g or amoxicillin??
Ampicillin + BLI for immunocompromised pts (if strep causes meningitis)
Penicillin-sensitive—amoxicillin, cefotoxime , ceftriaxone , cefprozil , macrolide
Penicillin-resistant-levo/moxifloxacin vancomycin , linezolid , telithomycin

Front 158

Streptococcus pyogenes
Gram + aerobic
Cocci

Back 158

pharyngitis, impetigo, necrotizing fasciitis

benzathine, penicillin V?, amoxicillin

Front 159

Listeria monocytogenes
Gram + aerobic
Bacilli

Back 159

foodborne illness, septicemia, meningitis

NOT 3rd gen cephs

Front 160

Nocardia asteroids
Gram + aerobic
Bacilli

Back 160

Skin
Tx w/ TMP/SMX DOC!

Front 161

Moraxella catarrhalis
Gram - aerobic
Cocci

Back 161

otitis media, RTI

ceph 3

Front 162

Neisseria gonorrhoeae
Gram - aerobic
Cocci

Back 162

genitals, meningitis

3rd gen cephs…

Front 163

Neisseria meningitidis
Gram - aerobic
Cocci

Back 163

Meningitis---
-Cef 3rd gen -cefotraixone, ceftazidime; ceftaxime enters CNS easier
chloramphenicol

Front 164

Bordetella pertussis
Gram- aerobic
Bacilli

Back 164

RTI (whooping cough)
azithromycin

Front 165

Campylobacter jejuni
Gram- aerobic
Bacilli

Back 165

GI

Front 166

Citrobacter
Gram- aerobic
Bacilli

Back 166

UTI

Front 167

Enterobacter
Gram- aerobic
Bacilli

Back 167

UTI, RTI

Front 168

Escherichia coli
Gram- aerobic
Bacilli

Back 168

UTI, RTI, GI
Rifaximin (non invasive strains, oral) in traveler’s diarrhea
UTI use nitrofuantoin
3rd gen-cefadroxil, cefazolin, cephalexin, cepharadine; TMP/SMX; ampicillin + sulfabactam?

Front 169

Francisella tularensis
Gram- aerobic
Bacilli

Back 169

skin, RTI

Front 170

Haemophilus influenza
Gram- aerobic
Bacilli

Back 170

RTI
Amoxicillin-oral and cefprozil-oral (if resistant) and cefuoxime-parenteral

Front 171

Helicobacter pylori
Gram- aerobic
Bacilli

Back 171

GI

amoxicillin, clarithromycin (DOC), tetracycline, metronidazole,

Front 172

Klebsiella pneumonia
Gram- aerobic
Bacilli

Back 172

RTI

Ceph 3-cefotaxime, ceftazidime, ceffriaxone; gentamicin

Front 173

Legionella pneumophila
Gram- aerobic
Bacilli

Back 173

RTI
erythromycin

Front 174

Proteus
Gram- aerobic
Bacilli

Back 174

GI
3rd gen cephs`

Front 175

Pseudomonas aeruginosa
Gram- aerobic
Bacilli

Back 175

RTI, UTI, wounds

Piperacillin and ticarcillin, cefipime (4th gen) all pareneral
meropeneml?
tobramycin (parenteral or topical)

Front 176

Salmonella
Gram- aerobic
Bacilli

Back 176

GI
ciprofloxacin

Front 177

Serratia
Gram- aerobic
Bacilli

Back 177

RTI, UTI
Carbapenams

Front 178

Shigella
Gram- aerobic
Bacilli

Back 178

GI
Carbapenams

Front 179

Vibrio Cholerae
Gram- aerobic
Bacilli

Back 179

GI; prevention: Cholera-close contacttetracycline

Front 180

Yesernia pestis
Gram- aerobic
Bacilli

Back 180

plaque

Front 181

Clostridium difficile
Gram + anaerobes
Bacilli

Back 181

GI (pseudomembranous colitis)

Front 182

Clostridium perfringens
Gram + anaerobes
Bacilli

Back 182

GI, gangrene

Front 183

Propionibacterium acnes
Gram + anaerobes
Bacilli

Back 183

Skin

Tretinoin, erythromycin,clindamycin

Front 184

Bacteriodes
Gram- anaerobes
Bacilli

Back 184

GI

Front 185

Borrelia burgdorferi
Atypical

Back 185

Lyme Disease-doxycycline DOC or piperacillin

Front 186

Chlamydia
Atypical

Back 186

Genitals NOT 3rd gen cephs!
Doxycycline (7 days) or azithromycin ; oral erythromycin for neonates (vertical transmission)

Front 187

Mycoplasma pneumonia
Atypical

Back 187

RTI
NOT 3rd gen cephs!

Front 188

Richettsia
Atypical

Back 188

Rocky Mt Spotted Fever--doxycycline

Front 189

Treponema pallidum
Atypical

Back 189

Syphilis—benzathine penicillin G; doxycylcine

Front 190

Bacilliary angiomytosis—bartonella henselase

Back 190

Erythromycin, doxycyline

Front 191

Anthrax

Back 191

Ciprofloxacin, doxycycline, penicillin G; even in suspected exposure

Front 192

Mycobacterium tuberculosis

Back 192

First-line drugs—Isoniazid, Ethambutol, Pyrazinamide, Rifampin, 2nd line—rifabutin, fluroquinolones, cycloseirne, capreomycin, ehtionamide, aminosalysylic acid w/ rifampin restiance—isoniazid, pyrazinamide, ethambutol, fluorquinolone; w/ isoniazid resistance rifampin, pyrazinamide, ethambutol, fluorquinolone;

Isoniazid + rifampin + pyrazinamide + ethambutol

Front 193

Mycobacterium avium intracellulare

Back 193

Prophylaxis-azithromycin-weekly; clarithromycin daily; tx-azithromycin + ehtambutol + rifabutin

Front 194

Mycobacterium leprae

Back 194

Tubuculoid-dapsone + rifampin; lepromatous-dapsone +rifampin + clofazimine

Front 195

talk about meningitis drugs

Back 195

Hib treatment: Ceph3+dex+vanco (note that we have not discussed dexamethasone, but it is given just prior to first dose of antibiotic)
Meningitis in newborns: empiric
<1 mo= AMP + ceph 3
>1mo= ceph3 + dex+ vanco
If know the bug, then: S. pneum= ceph3+vanco
N. menig= ceph3
L. monocytogenes= AMP
Neisseria= ceph3
Strep B= AMP +/- gentamycin

>50 or immunocompromised: AMP+ceph3+vanco+dex

What is most important is the trend, that is ceph3 is included more often than not and AMP is used in newborn and when L. monocytogenes or strep B. Vanco is included for more serious cases and in those that are immunocompromised.
Chloramphenicol treats all meningitis but causes gray baby syndrome

From CPS:
Emperical antibiotics-Premature infants and infants up to 3 mos-ampicillin+ cefotaxime, Children > 3 mos ,adults <55-cefotaxime+vancomycin, Adults>55 or with debilitating illnesses-ampicillin + cefotaxime +vancomycin, Dexamethasone 10mg iv 20 min before antibiotics the repeat q 6 hours for 4 days

Front 196

St. John’s Wort all

Back 196

Chemistry-From plant, Hypericum Perforatum , Active ingredients = hypericin & pseudohypericin
MAO-Mechanism is UNKNOWN, May block serotonin uptake (antidepressant action), May stimulate GABA receptors (anxiolytic)
anti-viral properties; BEST described best research ect! BEAT DEPRESSION not TREAT
Formulations-External use-ointment - warm leaves in hot petroleum jelly or beeswax, Fresh - apply leaves to wound, Internal-Capsules , Prepared teas, Tincture
“Therapeutic” uses-Major use is to treat mild to moderate depression, Acts as a combo GABA agonist and SSRI, Hypericin is the active component, Has been used as an anti-viral agent, Shown some effectiveness against retroviruses
SE and Toxicity-Phytotoxicity- ↑ sn to sunlight, HTN-Due to blockade of NE in addition to serotonin, nonselective
Things to Avoid-AA, tryptophan/tyrosine, Stimulants-- amphetamines, coffee, nasal decongestants, diet pills, cold/hay fever medication; Foods with Tyramine-wine, smoked/pickled foods, cheese, Other drugs--b2-agonists,

Front 197

st john's wort treats

Back 197

mild to mod depression as GABA agonist and SSRI

Front 198

SE of st john's wort

Back 198

HTN, sn to sun

Front 199

Panax Ginseng all

Back 199

First reported 2,000 years ago. From the Greek and Chinese words Meaning: “ALL HEALING MAN HERB”
Chemistry-Panax quinquefolius (American Ginseng), Panax ginseng (Asian), Active ingredients-panaxosides (American)
ginsenosides (Asian) - more potent; switching b/n American vs Asian may cause problems!
Mao-Anxiolytic activity. - Possibly via GABA receptor modulation in a fashion similar to benzodiazepines. Both red and white ginseng appear to decrease anxiety similar to diazepam. Takes 4-5 days for “therapeutic” effects, No apparent sedation or muscle relaxant activity
Formulations -External -capsules/tablets, prepared teas, freeze-dried root, dried root
‘Therapeutic’ uses-Treatment of depression , may be an anxiolytic (GABA) or SSRI, Panax Ginseng, Colds, influenza, respiratory problems, Damaged immune system,
Side effects/toxicity- may precipitate an asthma attack, heart palpitations or hypertension
Drug interactions-none reported

Front 200

most potent form of Ginseng

Back 200

asian-ginsenosides
vs
american-panaxosides

Front 201

ginseng treats?

Back 201

depression as GABA ag and SSRI, RTI; antianxiolytic

Front 202

SE of ginseng

Back 202

asthma attack, heart palpitations, HTN

Front 203

Ginkgo Biloba all

Back 203

Chemistry -Used for 1,000’s of years in China; From the plant - Ginkgo Biloba; NUT
Active ingredients-Leaves contain numerous active compounds , alcohols, aldehydes, ketones, terpenes, steroids, flavonoids, and glycosides; dozens of products
Physiological and Pharmacological Action -Dilates blood vessels, Increases cerebral & peripheral blood flow, Decreases cerebral glucose levels, Demonstrated to be neuroprotective in hypoxia and ischemia , scavenger of free radicals, Inhibits both MAO-A and B (anxiolytic), Possible synergistic action with antidepressants
Formulations –Capsules, Dried bulk, Tincture,
‘Therapeutic’ Uses -Vasculature disorder, Phlebitis, leg ulcers, cerebral atherosclerosis, diabetic vasculature disease, Mental/Emotional fatigue, Clotting disorders (stroke/MI), Headaches, Reynaud’s syndrome, Neuroprotectant, free radical scavenger
SE & Toxicity -Excessive bleeding or hemorrhage , Reports of ↑ cerebral bleeding in elderly patients

Front 204

ginkgo treats?

Back 204

vasculature disorders, ulcers, DM PVD, clots, HA, rauynauds b/c VD

Front 205

SE of ginkgo

Back 205

inc bleed esp cerebral bleed in elderly

Front 206

kava-kava all

Back 206

Chemistry-Grows as a bush (Piper methysticum) in South Pacific, referred to as the “intoxicating pepper” by John Cook
Active ingredients are: Kavain and Dihydrokavain, Methysticin and Dihydromethysticin
Physiological and Pharmacological Action-Biphasic, Stimulatory when CNS activity is low, Inhibitory when CNS activity is high, Possible active ingredients of Kava
Formulations -Capsules and prepared teas—may have CNS properties—euphoria and sense of well being
‘Therapeutic’ Uses-sedative, muscle relaxant, diuretic, anxiolytic ; secondary uses include: analgesia in place of aspirin, acetaminophen or other NSAIDS
Mode of action = UNKNOWN
Side effects-Acute - UNKNOWN , Chronic effects of Kava – eventually will become systemic; can make you sleepy, numbing of mouth and throat, poss block sodium channels; can make people sick

Front 207

kava-kava treats?

Back 207

sedative, mm relaxant, anxiolytic
analgesia

Front 208

kava-kava SE?

Back 208

unknown

Front 209

Valerian-

Back 209

Improve sleep - Do NOT use with benzodiazepines

Front 210

Cholestin-

Back 210

Red yeast fermented on rice - Lowers cholesterol

Front 211

Glucosamine and Chondroitin sulfates-

Back 211

From crab shells and cartilage -Usefulness ? cancer growth? May improve structure of joints

Front 212

Echinacea-

Back 212

Boosts immune system by ↑ WBC activity, not really significant

Front 213

Goldenseal

Back 213

-May act as antiseptic to treat sores in the mouth

Front 214

Dehydroepiandrosterone (DHEA)

Back 214

Androstenediol Testosterone
Biomarker that declines in the following-Normal aging, lupus, Alzheimer’s Disease, Cancer, Diabetes and Obesity
Supplementation as an ANTI-AGING “drug” is highly questionable
SE-Prolonged high doses can lead to liver dysfunction, ↓ CO, Masculinization of females
Lower doses (<25 mg/day) appear to have some beneficial effects (shouldn’t need it until 40 y.o.) just wanting to maintain, Weight loss, improved strength and endurance, improved cholesterol status (improved HDL/LDL), Improved mental alertness or cognition

Front 215

Melatonin

Back 215

Secreted by the pineal gland, responsible for regulation of the circadian rhythm, levels start to decline in middle age through old age, Sleep aid and to combat “jet-lag”
Best established use-Anti-Aging medication , No proven human studies that melatonin reverses the aging process, April 1997; the NIA speaks against anti-aging med’s;
Side effects include infertility and loss of libido