Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/35

Click to flip

35 Cards in this Set

  • Front
  • Back
Describe the general Aminoglycosides –Structure, Use, Route
Polar cations made of Amino sugars attached to amiocylitol ring by glycosidic link
Reserved mostly for serious G- & Used with B-lactams for synergistic effect/G+ coverage
Parenteral use – IV usually
Mechanism of synergism of Aminoglycosides w/ B-lactams:
Inhibiting cell wall synthesis (b-lactam) increases penetration of aminoglycosides
SE of Amioglycosides
Nephotoxic & Ototoxic, excreted by kidney so dose adjusted for renal function. OTOXIC in neonates = caution if pregnant, as accumulates fetal plasma
Can cause Neuromusclular block (resp paralysis) due to decrease Ach Release.
How do you Tx respitory paralysis as a side effect of Aminoglycosides?
Need to correct the problem caused by decease in Ach release
Give IV Ca+ or neostigmine (cholinesterase inhibitor, allowing the Ach to act for longer period of time before degradation)
Mechanism of Aminoglycosides:
Enter periplasmic space of G- through porin channels.
Pass Thru inner membrane by flowing down electrochemical gradient
How does the action of Aminoglycosides change with dosage?
Static effects dependent upon concentration
-Low levels cause misreading of mRA  faulty proteins
-Higher levels inhibit initiation of transcription  no proteins
Cidal when faulty proteins (made during low dosage) insert into cell membrane, causing leaking ions & proteins
Where are the highest level of aminoglycosides attained?
-Renal Cortex  Nephrotoxicity
Reversible as tubular cells regenerate
-Edolymph  Ototoxicity
Irreversible – sensory hairs don’t grow back
Mech: Could disrupt ion flow or some other mech; unknown for sure
Degeneration of auditory nerve permanent hearing loss
Name 3 aminoglycosides given by IV & their uses
Genatmicin – topical for superficial eye infect, for burns & wounds, and to prevent catheter infec.
Tobramycin – same uses as gentamicin, sometimes combined with dexamethasone (anti-inflamm) for G- eye infect
Amikacin – Nosocomial infections that resist gentamicin & tobramicin
Name 3 oral aminoglycosides and their uses
Kanamycin – for prep for bowel surgery. Can also be used IV
Neomycin – for prep for bowel surgery & topical anti-infectant
Paromomycin – DOC for amebic dysentery (protozoa Entamoeba histolytica)
What are the 2 ways to adjust dose for Renal Fcn?
1) increase or decrease dose
2) change dosing interval
What is Creatinine clearance? Use? Units? What’s “normal” level?
Time to clear creatinine from kidney, used to determine renal function
Expressed in ml/min – normal is 125 ml/min
What is the Cockcroft-Gault equations & what is it used for?
How is it altered for women?
(140-age) x (lean wt in kg)
------------------------------
72 x [Serum creatinine, mg/dl]

– to estimate Creatinine clearance

For women, multiply by 0.85
How is Lean Body Weight (LBW) calculated?
Male= 50 KG + 2.3 kg for each inch over 5 ft
Female = 45.5 + 2.3 kg for each inch over 5 ft
How do you determine the Aminoglycoside dose for a patient when taking Renal fcn into acct?
Max daily dose x estimated Cl
-----------------------------
125 ml/min
What do the terms “desired peak level” and “trough” level refer to?
Are these levels the same for all the IV aminoglycoside?
Peaks level is [drug] 30-60 min after dose, trough just before next dose
No, Amikacin has very different desired peak level than gent & tobra
(don’t need to know specifics)
What is the general structure of Tetracylines? Use?
4 rings
Broad spectrum 2nd line against G+ & G-
What is the Mech of Tetracyline?
Inhibits binding of aminoacyl tRNA to acceptor site of ribosome - Static by preventing translation
Name a short-acting Tertracycline. What is its “half-life”? Use?
Short acting: T ½ = 6-8 hrs
Tetracycline (Rx) – Alternate oral or topical for inflammatory acne
(1st DOC topical erythromycin + benzoyl peroxide)
Name an intermediate acting Tetracycline? What is its “half-life”? Use?
Intermediate Acting: T ½ ~ 12 hrs)
Democlocyine – Used to treat chronic dilutional hyponatremia assoc with Syndrome of Inappropriate ADS secretion (water retetion)
Name a Long Acting Tetracyline? What is its “half-life”? Use?
Long acting: T ½ = 16-18 hrs
Doxycycline – Oral & IV
1st DOC for Ricketsia (Rocky Mt Spot Fever), Chlamydia trachomatis, lyme disease. Alt for Syphilis c/ PCN allergy (Fluorquinolone DOC)
What stomach contents inhibit tetracycline absorbtion?
Dairy products & antacids – causes chelations by the calcium or metallic salts
What is the mechanism of Tetracyclines?
??????? I missed this somehow??? Help?
SE of Tetracylines:
-GI upset
-Photosensitivity
-Permanent brown discoloration of teeth
What is Tigecycline – drug or class? Mech? Use?
Class similar to tetracyclines & might have similiar effects. Same mech of tetracyclines. Use: MRSA & tetracycline sensitive G-/G+, complicated skin & intra-abd infection
Describe structure of Macrolides. Effective against?
Large lactone ring w/ 1+ deoxy sugars.
All are effective against MSSA, Moraxella catahhralis, H. influenzae
Describe the Main Mech of Macrolides
Inhibits translocation of tRNA from acceptor to donor site of ribosome, thus preventing protein translation
Name 3 Macrolides
Erythromycin
Azithromycin
Clarithromycin
Erythomycin: Route? 5 Salt versions? Which salt best absorbed?
Usually oral, EC = enteric coated free base
5 salt versions available: estolate, stearate, ethylsuccinate, lactobionate, gluceptate
Best absorbed: Estolate salt, but can  cholestatic hepatic
Erythromycin was the 1st Rx effective against what? How is it used now?
1st vs Legionnaires’ – now Azithromycin or Levofloxacin are DOC & erythro is alternate
Erythro DOC for Pneumonia for Campy jejuni, Conyne diphtheria, Boredetella pertussis
Erytho is a component of Pediazole for Otitis Media (along with sulfisoxazole)
What are the SE of Erythromycin?
-Metabolites complex c/ cytochrome heme Fe & inhibit CYP3A, decreasing erythro metabolism
-Can prolong cardiac repolarization  torsades arrhythmia. Incr risk if used with other Rxs that inhibit CYP3A (incr. erythro level)
-Doubles risk of sudden cardiac death. Risk increases 5x with concurrent use of diltiazem or verapamil (CV drugs, anti-arrhythmic drug)
Azithromycin is in which class? Use?
Macrolide used for community acquired pneumonia, legionnaires, Chlamydia trachomatics, Mycobac avium, & alt for Bordetella pertussis
What is the “Half-life” of Azithromycin? Metabolism?
T ½ = 70 hrs. Concentrates intracellularly. Doesn’t inhibit P450. Excreted unchanged in bile
Use of Clarithromycin? SE?
For comm. Acquired pneumonia & Mycobac avicum & is part of a “tx cocktail” forH. Pylori.
SE: Has caused low blood sugar & does inhibit CYP3A (incr Rx level)
Describe Ketolide
New class – a macrolide derivative with incr G+ activity.
Mech same as macrolides
Name one Ketolide. Use? Concentrates where?
Telithromycin used for comm. acquired resp infect. Active vs B-lactam & macrolide resistant bugs but some resistance is already forming. Concentrates in pul tissues & WBC.