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88 Cards in this Set

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IPS = ?
Inhibitors of Protein Synthesis
What do the IPS's target?
70S Ribosome (vs. 80S for humans)
Mnemonic for IPS's
buy AT 30, CELL at 50

30S inhibitors
- A = Aminoglycosides
- T = Tetracyclines

50S inhibitors
- C = Chloramphenicol
- E = Erythromycin
- L = Lincomycin
- L = cLindamycin
What is the only IPS that is BACTERICIDAL? Why?
Aminoglycoside b/c it binds irreversibly
Why are IPS's substantially less Selectively Toxic than ICWS?
b/c IPS's take advantage of structural differences in the pathogen to get selective effects while ICWS's take advantage of a unique target
Tetracycline mechanism of action
- REVERSIBLE binding to 30S subunit = Bacteriostatic
- block the attachment of aminoacyl tRNA to the acceptor site
How is Tetracycline usually administered?
Orally, but absorption is variable basd on what else is in the GI tract

*rarely given IV
What is the caveat when giving Tetracycline orally? Why?
Do not give with Milk, food, antacids b/c they chelate with metal ions
- not absorbed
- lose antibiotic ability
Describe the distribution of Tetracycline
1. well distributed, except CNS and synovial fluid

2. concentrates in TEETH and BONE, liver, and kidney
What 2 groups of people should you never give Tetracycline to and why?
Children and Pregnant/breast-feeding mothers

b/c tetracycline crosses the placenta and is excreted in milk
- teeth discoloration
- inhibits bone growth
How are most Tetracyclines excreted? What is the exception?
1. in Urine

2. Doxycline is more lipid-soluble = fecal
What type of patients can Doxycline be given to and why?
Those with Renal Failure b/c it is excreted fecally
What is the mnemonic for the clinical uses of Tetracycline?
VACUUM THe BedRoom = Gram +/-

V = vibrio cholera
A = Acne
C = Chlamydia
U = Ureaplasma
U = Urealyticum
M = Mycoplasma pneumoniae
T = Tularemia
H = H. pylori
B = Borrerlia burgdorferi (Lyme Disease)
R = Rickettsia
List the 5 adverse effects of Tetracycline and why
1. GI = direct irritation b/c given orally

2. Superinfections b/c of broad spectrum

3. Impaired liver fxn due to high doses, during pregnancy, or pre-existing liver disease

4. Photosensitivity

5. Calcium chelation
-teeth discoloration
-inhibits bone growth
List 2 ways that resistance to Tetracycline occurs
1. Efflux pumps (plasma-mediated)

2. altered ribosomal proteins
Which microbes commonly have altered ribosomeal proteins that allows resistance to Tetracycline?


*don't use Tetracycline for these
What has fostered the emergence of resistance to Tetracycline
Overuse clinically and AGRICULTURALLY
Name for the new generation of Tetracyclines
What is better about the Glycylcyclines?
retain antibacterial spectrum of tetracyclines but overcome the resistance
What tetracycline is not affected by efflux pump except in Proteus and Pseudomonas?
Tetracycline that has a particular usefulness in Prostatitis because it reaches high levels in prostatic fluid
Tetracycline that appears at high levels in Saliva and is used in the Meningococcal carrier state
Used in the Syndrome of Inappropriate secretion of ADH b/c it blocks the ADH receptor fxn in the collecting ducts and acts as a diuretic
What is Chloramphenicol's mechanism of action?
REVERSIBLE inhibitor of 50S
- inhibits the formation of the Peptide Bond = inhibits Peptidyltransferase
Protein systhesis inhibitor that is well absorbed from ALL routes -> CNS levels = Serum levels
IPS that has these excretion pharmacokinetics:

100% excreted in urine
- 10% filtration of parent
-90% tubular secretion of glucuronide
What is the rate-limiting step in Chloramphenicol clearance?
Glucuronidation in the liver
Describe the resistance to Chloramphenicol
- Plasmid-mediated
- Chloramphenicol Acyl Transferase
-Slow development and only slight resistance so increasing the dose 2-4X works
List the 5 Adverse effects of Chloramphenicol
1. GI disturbances followed by Fungal Superinfections
2. Anemia due to bone marrow depression
3. Aplastic anemia
4. Gray Baby Syndrome
5. Drug-drug interactions = inhibits microsomal enzymes

ChlorineAM pool has a Gray baby in it who has GI fungal infection, 2 types of anemia, and inhibits CYP
Describe Anemia due to bone marrow depression due to Chloramphenicol
-Arrested Red cell maturation
-Dose and time related
-usually reversible
Describe Aplastic Anemia due to Chloramphenicol
- idiosyncratic rxn (1 in 35,000)
Why does Gray Baby Syndrome occur in neonates taking Chloramphenicol?
they have immature livers = poor Glucuronidation = low clearance = high toxicity

*lack liver UDP-glucuronyl transferase
What drugs does Chloramphenicol inhibit the metabolism of? (3)
1. Phenytoin
2. Sulfonylureas
3. Warfarin

**Chloram pool has SulferPee in it to make it look like a FUNNY-WARF
What is the clinical use of Chloramphenicol?
limited use due to toxicity but used in children for:
- Typhoid Fever

*b/c you don't want to give Tetracycline
Mnemonic for Macrolide antibiotics
mACE (all end in -thromycin

A = Azithromycin
C = Clarithromycin
E = Erythromycin
Macrolide mechanism of action
Bind to 23S rRNA of 50S subunit
- inhibit translocation of peptidyl-tRNA from acceptor site to donor site
Macrolide: static or cidal?
Either, depends on dose
Describe the absorption of Macrolides
Absorbed fro GI tract but ACID-labile
-use enteric coating capsule
- Erythromycin esters = acid-stabile
IPS that has excellent distribution except to the CNS but CROSSES the Placenta
Macrolides = mACE
Describe the excretion of Macrolides
excreted in Bile = levels are 50X higher than in plasma
What is the half-life of Macrolides? Exception?
2-5 hrs

Azithromycin = 2-4 days
List the 3 Adverse Effects of Macrolides
1. GI distress (stimulates motilin receptors) = nausea

2. Hepatoxicity
-Erythromycin estolate -> Cholestatic jaundice

3. Microsomal enzyme inhibition
-Warfarin, coumadin
-non-sedating anti-histamines
MacroLiar (think Liar Liar) has 1) upset stomach 2) cholestatic jaundice (yellow) 3) Inhibits metabolism of: WAR DIGs at HISTAMINa
Clinical uses for Macrolides
Gram +, some Gram -, some Mycobacteria

*backup for Penicillins in Pen-sensitive patients
*also for Mycoplasma pneumonia, Legionnaire's disease, Chlamydia
**Macrolides = MCL
Which Macrolides are Broader Spectrum? What are they used to treat?
Azithromycin = sinusitis or otitis media (H. influenza, M. catarrhalis), Chlamydia, MAI


Clarithromycin = increased activity against MAC and H. pylori
What microbes may be Macrolide-resistant?
1. Staph
2. some Strepto
3. Pneumococci (Strep pneumo)
What are the 2 ways microbes attain resistance to Macrolides?
Both plasmid-mediated
1. Methylated rRNA

2. Esterase which hydrolyzes Erythromycins
What is the advantage of Clarithromycin?
Has less GI effects

**Clair Green has less GI effects
2 advantages of this IPS are:

1. minimal P450-based interactions

2. tissue level 10-100X plasma levels = longer half-life = 2-4 days vs. 2-5 hrs.

*longer half-life than other Macrolides
What is Azithromycin particularly active against?
Mycobacterium avium-intracellulare (MAI) in AIDS patients
What category of drug does Clindamycin fall in?
Clindamycin: static or cidal?
Describe the distribution of Clindamycin
well absorbed and distributed except for CNS
Clinical uses of this drug are:
1. Anaerobes = Bacteroides fragilis, C. perfringens
2. Endocarditis prophylaxis
3. Orthopedic surgical cases
What are 3 Adverse Effects of Clindamycin?
1. GI upset

2. C. difficile superinfection = Pseudomembranous colitis

3. Hepatotoxic
List the two Sterptogramins and their trademark name
Quinupristin and Dalfopristin

How are the Streptogramins administered and why?
IV b/c they're too big to be absorbed orally = peptide macrolactones
How are the Streptogramins (Quinpristin & Dalfopristin) excreted?
80% bile

20% urine
What is the drawback to Streptogramins
potent inhibitor of CYP 3A4 = major metabolizer of prescription drugs
IPS that is CIDAL to all organisms except E. faecium (bacteriostatic)
Streptogramins = Quinupristin & Dalfopristin
What are the Streptogramins (-pristins) clnically used for?
Vanco and multi-drug resistant E. faecium

What is the only relevant drug in the Oxazolidinones group?
Linezolid mechanism of action
prevents formation of 70S ribosome = unique mechanism
Why does Linezolid have no cross-resistance with other IPS's
b/c it inhibits a unique mechanism
What is Linezolid CIDAL against?

What is it STATIC against?

Staphylococci and Enterococci
How is Linezolid administered?
IV or Oral

*oral AUC = IV AUC
What is the primary clinical use for Linezolid?
VRE (Vancomycin resistant Entercocci)
What are the 2 adverse effects of Linezolid?
1. Bone Marrow suppression

2. Thrombocytopenia
Aminoglycosides: Cidal or Static?
CIDAL = irreversible inactivation of 30S
IPS that has these actions:
1. interfere with formation of initiation complex
2. misreading of mRNA
3. break up polysomes
What is the mnemonic for the drugs in the Aminoglycoside class?
"mean" GNATS canNOT kill anaerobes

G = Gentamicin
N = Neomycin
A = Amikacin
T = Tobramycin
S = Streptomycin

N = Nephrotoxicity
O = Ototoxicity
T = Teratogen
How are Aminoglycosides administered and why?
Usually IV, sometimes IM
- poor oral absorption b/c they are polar amino sugars
Describe the distribution of AmINoglyCoSides
Good except for eye and CNS
How are Aminoglycosides excreted
UNCHANGED by glomerular filtration
Where can Aminoglycosides collect in very high concentrations?
Proximal tubule cells
What are the clinical uses for Aminoglycosides
non-resistant Gram - infections
-E. coli
What is the order of drug use for Pseudomonas?
Carbenicillin > gentamicin > tobramycin > amikacin

**just like DNA bases: CG-TA
What is the general rule when prescribing Aminoglycosides?
Use OLDER ones first and save newer one for when they are needed
What are the 2 older Aminoglycosides?
Streptomycin and Gentamicin
- use first

**Senile Gent**
Why are Aminoglycosides ineffective against Anaerobes?
b/c they require O2 for microbe uptake (uptake mechanism is dependent on oxygen)
Group of drugs related to Aminoglycosides that are used against Penicillin-resistant Gonococci (N. gonorrhoeae)
What is the toxicity of Aminoglycosides dependent on?
Both time and blood level

*most drugs are just based on blood level
IPS that is used by "once daily" dosing

= give a very high dose of drug which causes a high spike, high killing, but minimizes toxicity due to decreased time in blood
What are the 3 adverse effects of Aminoglycosides?
1. Nephrotoxicity
2. Ototoxicity
3. Neuromuscular blockade
Where does Aminoglycoside concentrate in the Kidney?

After how many days do 5-25% of people taking AG show progressive renal impairment?
Renal Cortex

3 days
By what 4 drugs is the Nephrotoxicity of Aminoglycosides exacerbated?
1. Vancomycin
2. Cyclosporin
3. Amphotericin B
4. Cisplatin

When is the adverse effect of Neuromuscular Blockade most common with Aminoglycosides?
-during surgery with the presence of other neuromuscular blockers
-Myasthenia gravis patients

*high dose phenomenon
What happens if Aminoglycosides are administered alone?
microbes RAPIDLY develop resistance
List 3 ways in which microbes may become resistant to Aminoglycosides
1. Increased BACTERIAL metabolism = adenylation, acetylation, phosphorylation

2. Alteration in bacterial uptake
-altered transport system

3. Altered ribosomal protein