Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
236 Cards in this Set
- Front
- Back
Pharmacokinetics
|
p. 288
|
|
amount of drug in body/_______ = Vd
|
plasma drug concentration (note: Vd is Volume of Distribution)
|
|
rate of elimination of drug/[plasma drug] = ?
|
CL (Clearance)
|
|
(.7)(Vd)/CL = ?
|
T 1/2
|
|
A drug infused at a constant rate reaches about 94% of steady state after _______ t 1/2s.
|
4
|
|
Dosage Calculations
|
p. 288
|
|
A loading dose is calculated using this formula.
|
(Cp)(Vd)/F (note: Cp = target plasma concentration, and F = bioavailability)
|
|
A maintenance dose is calculated using this formula.
|
(Cp)(CL)/F
|
|
Elimination of Drugs
|
p. 288
|
|
Rate of elimination is proportional to _______ ______ in 1st order elimination.
|
drug concentration
|
|
In the case of EtOH, which is elimated by _____ order elimination, a constant amount of drug is eliminated per unit time.
|
zero
|
|
Phase I vs. Phase II metabolism
|
p. 289
|
|
Phase ____ (I or II) reactions yield slightly polar metabolites that are often _____ (active or inactive)
|
I, active
|
|
Phase ____ (I or II) reactions yield very polar metabolites that are often _____ (active or inactive) and are excreted by the _______.
|
II, inactive, kidney
|
|
Phase II reactions are often of this type.
|
conjugation
|
|
Cytochrome P-450 is involved in _____ phase (I or II) reactions.
|
I
|
|
Drug Development
|
p. 289
|
|
A patent lasts for _____ years after filing for application.
|
20
|
|
How many phases are there in drug development?
|
4
|
|
Drugs are first tested in patients in phase _____ of clinical testing, pharmacokinetic safety is determined in phase ______ of clinical testing, double blind tests are done in phase ____ and post-market surveillance is done in phase _____.
|
2,1,3,4
|
|
Pharmacodynamics
|
p. 289
|
|
In a dose response curve, a competitive antagonist shifts the curve _____, while a non-competitive antagonist shifts the curve ______.
|
right, down
|
|
AUTHOR
|
HiralShah
|
|
Pharmacodynamics (continued)
|
p. 290
|
|
What pharmacologic relationship would determine the existence of spare receptors?
|
EC50 < Kd
|
|
What does it mean if EC50 and Kd are equal?
|
The system does not have spare receptors
|
|
A partial agonist acts on the same receptor system as a full agonist? T/F
|
TRUE
|
|
What's the main difference between a partial agonist and a full agonist?
|
A partial agonist has a lower maximal efficacy.
|
|
Is a partial agonist less potent than a full agonist?
|
Not necessarily. It can be less, more or equally potent as a full agonist.
|
|
Antimicrobial Tx -- Mechanism of Action
|
p. 291
|
|
The penicillin type drugs work by blocking ------ synthesis, specifically by inhibiting this molecule from cross-linking?
|
blocks bacterial cell wall synthesis by inhibition of peptidoglycan synthesis.
|
|
Which other drugs (aside from penicillin) have this same mechanism of action?
|
Imipenem, aztreonam and cephalosporins
|
|
Bacitracin, vancomycin and cycloserine block the synthesis of this molecule, preventing cell wall synthesis
|
peptidoglycans
|
|
These drugs block the 50s ribosomal subunit
|
clindamycin, chloramphenicol, erythromycin, lincomycin, linezolid, streptogramins "Buy AT 30, CELL at 50"
|
|
These drugs block the 30s ribosomal subunit
|
Aminoglycosides and tetracyclines "Buy AT 30, CELL at 50"
|
|
These drugs block nucleotide synthesis by interfering with the folate pathway
|
Sulfonamides (e.g. Bactrim), trimethoprim
|
|
These drugs block DNA topoisomerases
|
Quinolones (e.g. Cipro)
|
|
Which drug blocks mRNA synthesis
|
rifampin
|
|
Which are the bacteriacidal Abx
|
Penicillin, cephalosporin, vancomycin, aminoglycosides, fluoroquinolones, metronidazole
|
|
These drugs disrupt the bacterial/fungal cell membranes
|
polymyxins
|
|
These specific disrupt fungal cell membranes
|
amphotericin B, nystatin, fluconazole/azoles (FAN the fungal cell membranes)
|
|
What is the mechanism of action of Pentamidine
|
Unknown
|
|
Penicillin
|
p. 291
|
|
Which is the IV form and which is the oral form
|
G = IV, V=oral
|
|
Which of these is not a mechanism of penicillin action: (1) binds penicillin-binding protein, (2) blocks peptidoglycan synthesis, (3) blocks transpeptidase catalyzed cross-linking of cell wall and (4) activates autolytic enzymes
|
Penicillin does not block peptioglycan synthesis, bacitracin, vancomycin and cycloserine do that
|
|
T or F: penicillin is effective against gram pos and gram neg rods
|
False: penicillin is used to treat common streptococci (but not staph), meningococci, gram pos bacilli and spirochetes (i.e. syphilis, treponema). Not used to treat gram neg rods.
|
|
What should you watch out for when giving penicillin?
|
Hypersensitivity rxn (urticaria,severe pruritus) and hemolytic anemia
|
|
Methicillin, nafcillin, dicloxacillin
|
p. 291
|
|
These drugs are used mainly for what type of infection
|
Staphlococcal infection (hence very narrow spectrum)
|
|
T or F: these drugs have the same mechanism of action as penicillin
|
TRUE
|
|
Are these drugs penicillinase resistant? If so why?
|
Bulkier R group makes these drugs resistant to penicillinase
|
|
What should you watch out for when giving these drugs?
|
Hypersensitivity rxn (urticaria,severe pruritus); methicillin can cuase interstitial nephritis
|
|
Ampicillin and amoxicillin
|
p. 291
|
|
T or F: these drugs have the same mechanism of action as penicillin
|
TRUE
|
|
Which has greater oral bioavailability?
|
amOxicillin (O for Oral)
|
|
What do you use these for?
|
Ampicillin/amoxicillin HELPS to kill enterococci (H. influenzae, E. coli, Listeria monocytogenes, Proteus mirabilis, Salmonella)
|
|
Can penicillinase effect these drugs efficacy?
|
Yes, they are penicillinase sensitive
|
|
Why not give these drugs with a penicillinase inhibitor. Name one.
|
clavulanic acid
|
|
What should you watch out for when giving these drugs?
|
Hypersensitivity rxn (ampicillin rash), pseudomembranous colitis
|
|
Carbenicillin, piperacillin, ticarcillin
|
p. 292
|
|
Why are these considered to have an extended spectrum?
|
Because they are effective against pseudomonas and other gram neg rods (enterobacter and some species of klebsiella)
|
|
What should you watch out for when giving these drugs?
|
Hypersensitivity rxn
|
|
Why does concomitant administration with clavulanic acid increase the efficacy of these drugs?
|
Because they are penicillinase sensitive. (only piperacillin and ticarcillin)
|
|
Cephalosporins
|
p. 292
|
|
What is the mechanism of action of Cephalosporins?
|
inhibit cell wall synthesis
|
|
How are they similar/different from penicillin?
|
both have a beta-lactam ring structure but cephalosporins are less susceptible to penicillinases
|
|
What are the main similarities/difference between 1st and 2nd generation cephalosporins?
|
2nd gen has extensive gram neg coverage but weaker gram pos coverage
|
|
1st gen covers what bugs?
|
gram positives (staph and strep), Proteus mirabilis, E. coli, Klebsiella (PEcK)
|
|
2nd gen covers what bugs?
|
gram positives (staph and strep) though less so, H. influenzae, Enterobacter aerogenes, Neisseria, Proteus mirabilis, E. coli, Klebsiella (HEN PEcK)
|
|
What can 3rd generation drugs do that 1st and 2nd generation can't?
|
Cross the blood brain barrier
|
|
What are some other benefits of 3rd gen?
|
better activity against gram neg bugs resistant to beta-lactam drugs. Ceftazidime for Pseudomonas and ceftriaxone for N. gonorrhea
|
|
What are the benefits of 4th gen (e.g. Cefipime)?
|
increased activity against Pseudomonas, gram pos organisms and more beta-lactamase resistant (i.e. 4th gen combines 1st gen and 3rd gen characteristics into super drug)
|
|
What drugs should you avoid taking with cephalosporins?
|
Aminoglycosides (increases nephrotoxicity) and ethanol (causes a disulfiram-like rxn -- headache, nausea, flushing, hypotension)
|
|
Aztreonam
|
p. 292
|
|
When would you use aztreonam?
|
Only to treat Klebsiella, Pseudomonas and Serratia spp.
|
|
Is it beta-lactamase resistant?
|
Yes, this is one of the huge benefits of the drug, and it is not cross-reactive with PCN!
|
|
Which population of pt. is this drug good for?
|
The PCN-allergic patient that can't take aminoglycosides b/c of renal insufficiency
|
|
Are there any toxicity issues with this drug?
|
Not really. Generally well tolerated with occasional GI upset. Vertigo, Headache and rare hepatotoxicity have been reported.
|
|
Imipenem/cilastatin
|
p.293
|
|
What is imipenem?
|
broad spectrum beta-lactamase-resistant abx
|
|
What do you always administer it with and why?
|
cilastatin -- it decreases inactivation of imipenem in renal tubules
|
|
What do you use it for?
|
Gram pos cocci, gram neg rods and anaerobes (broad spectrum)
|
|
What bug is it the drug of choice for?
|
Enterobacter
|
|
What are its side-effects
|
GI distress, skin rash, seizures at high conc.
|
|
Vancomycin
|
p. 293
|
|
Is it bactericidal or bacteriastatic and why?
|
Bactericidal because it blocks cross linkage and elongation of peptidoglycan by binding D-ala D-ala protion of cell wall.
|
|
How does resistance to Vanco occur?
|
D-ala D-ala is replaced with D-ala D-lactate which vanco does not block
|
|
What is it used for?
|
Used for serious infection that is resistant to other drugs (e.g. gram pos multi-drug resistant organisms like S. aureus and C. difficile, methicillin resistant staph (MRSA))
|
|
What are the important toxicities of vanco?
|
generally NOT many problems except, Nephrotoxicity, Ototoxicity and Thrombophlebitis
|
|
What can happen with rapid infusion of vanco?
|
Red man's syndrome. Diffuse flushing which can be controlled by pretreatment with anti-histamines and with slow infusion rate
|
|
Protein Synthesis Inhibitors
|
p. 293
|
|
Which drugs target bacterial protein synthesis by blocking the 30S unit vs 50S unit?
|
Buy AT 30, CELL at 50
|
|
What does AT stand for?
|
A = Aminoglycosides (streptomycin, gentamicin, tobramycin an damikacin. And T = Tetracyclines
|
|
What does CELL stand for?
|
C = Chloramphenicol, E= Erythromycin, L= Lincomycin and L= cLindamycin
|
|
Which of the above are bactericidal?
|
Only the aminoglycosides are, the rest are bacteriostatic
|
|
Aminoglycosides
|
p. 294
|
|
Name some aminoglycosides?
|
Gentamicin, neomycin, amikacin, tobramycin and streptomycin
|
|
How do these drugs work?
|
They inhibit formation of the initiation complex in mRNA translation
|
|
Why are they ineffective against anaerobes?
|
They require oxygen for uptake into bacteria
|
|
When would you use aminoglycosides?
|
against severe gram-negative rod infections
|
|
What drugs can you use aminoglycosides with for synergy?
|
the drugs that inhibit cell wall synthesis (e.g. penicillin and cephalosporins -- the beta-lactam antibiotics). Presumably this allows the drug to get in with out reliance on oxygen transport
|
|
What drug in this class is commonly used for bowel surgery?
|
Neomycin
|
|
What are the two major toxicities?
|
Nephrotoxicity (esp. when used with cephalosporins) and Ototoxicity (esp. when used with loop diuretics). amiNOglycosides
|
|
Tetracyclines
|
p. 294
|
|
Name some tetracylcines
|
Tetracycline, doxycycline, demeclocycline, minocycline
|
|
How does it work?
|
Blocks t-RNA attachment to 30S subunit
|
|
Which tetracycline can you use in patients with renal failure and why?
|
Can use doxycycline because its elimination is fecal
|
|
Should you take these drugs with a glass of milk?
|
NO, because it intereferes with absorption in the gut as does antacids and iron-containing preparations
|
|
What are tetracyclines used for?
|
VACUUM your Bed Room -- Vibrio cholerae, Acne, Chlamydia, Ureaplasma, Urealyticum, Mycoplasma pneumoniae, Borrelia burgdorferi, Rickettsia, tularemia
|
|
What are the common toxicities
|
GI distress, teeth discoloration, inhibition of bone growth in children, Fanconi's syndrome and photosensitivity
|
|
Macrolides
|
p. 294
|
|
Name some macrolides?
|
Erythromycin, azithromycin, clarithromycin
|
|
How do these drugs work?Macrolides
|
inhibit protein synthesis
|
|
What are Macrolides used for?
|
URIs, pneumonias, STDs -- gram pos cocci in patients that are allergic to PNC --- Mycoplasm, Legionella, Chlamydia, Neisseria.
|
|
Pneumonic for macrolide use?
|
Eryc's Nipple is at his Mid Clavicular Line (Eryc is brand name for erythromycin). Mycoplasm, Legionella, Chlamydia, Neisseria.
|
|
What are the major toxicities?Macrolides
|
GI discomfort, acute cholestatic hepatitis, eosinophilia, skin rashes
|
|
What is the most common cause for non-compliance to macrolides?
|
GI discomfort
|
|
Chloramphenicol
|
p. 294
|
|
How does Chloramphenicol work?
|
inhibits 50S peptidyltransferase
|
|
Main use?
|
Meningitis (H. influenzae, N. meningitides, S. pneumo). Used conservatively b/c of toxicity
|
|
What are the main toxicities?
|
Anemia and aplastic anemia (both dose dependent), gray baby syndrome (in premes b/c they lack UDP-glucoronyl transferase)
|
|
Clindamycin
|
p. 294
|
|
How does it work?
|
blocks peptide bond formation at 50S
|
|
When do you use it?
|
Anaerobic infections (e.g. Bacteroides fragilis and C.perfringens)
|
|
Toxicities?
|
Pseudomembranous colitis, fever, diarrhea
|
|
Sulfonamides
|
p. 295
|
|
Name some sulfonamides
|
Sulfamethoxazole (SMX), sulfisoxazole, triple sulfa and sulfadiazine
|
|
How does it work?
|
Inhibits bacterial folic acid synthesis from PABA by blocking dihydropteroate synthase.
|
|
What are its uses?
|
Gram-positive, gram-negative, Nocardia, Chlamydia. Triple sulfas and SMX for simple UTIs
|
|
Toxicities?
|
hypersensitivity rxn, hemolysis if G6PD deficient, nephorotoxicity (tubulointerstitial nephritis), kernicterus in infants, displace other drugs from albumin (e.g. warfarin)
|
|
Trimethoprim
|
p. 295
|
|
How does it work?
|
inhibits folic acid pathway by blocking dihydrofolate reductase which humans have as well
|
|
What are its uses?
|
used in combo with Sulfamethoxazole (TMP-SMX) causing a sequential block of folate synthesis. Used for recurrent UTIs, Shigella, Salmonella, and prophylaxis for PCP in AIDS patients
|
|
Toxicities?
|
Megaloblastic anemia, pancytopenia (may be alleviated with supplemental folinic acid)
|
|
Fluoroquinolones
|
p. 295
|
|
What the most famous floroquinolone?
|
Ciprfloxacin (treatment for Anthrax)
|
|
How does it work?
|
inhibits DNA gyrase (topoisomerase II)
|
|
What are its uses?
|
Gram neg rods or urinary and GI tract (incl. pseudomonas), Neisseria, some gram pos spp
|
|
What population is contraindicated for use?
|
pregnancy and children
|
|
What are its toxicities?
|
GI upset, superinfection, skin rashes, headache, dizziness and tendonitis and tendon rupture in adults. FluoroquinoLONES hurt attachment to BONES.
|
|
Metronidazole
|
p. 296
|
|
How does it work?
|
forms toxic metabolites in the bacteria. Bactericidal.
|
|
What are its uses?
|
anti-protozoal: Giardia, Entamoeba, Trichomonas, Gardnerella vaginalis, anaerobes (bacteroides, clostridium)
|
|
What is the role of Metronidazole in H. pylori infection?
|
Used as part of triple therapy: bismuth, amoxicillin and metronidazole
|
|
Main toxicity?
|
disulfiram-like (antabuse) reaction to alcohol and headache
|
|
Which drug do you use to treat anaerobic infections above the diaphram and below the diaphram
|
anaerobes above diaphram: Clindamycin, and anaerobes below diaphram: metronidazole
|
|
Polymyxins
|
p. 296
|
|
How does it work?
|
disrupts osmotic properties of bacteria, acts like a detergent
|
|
What is it used for?
|
resistant gram negative infections
|
|
Toxicities?
|
neurotoxicity, ATN
|
|
Isoniazid
|
p. 296
|
|
How does it work?
|
decreases synthesis of mycolic acid
|
|
What is it used for?
|
MTB (mycobacterium tuberculosis). The only agent used as solo prophylaxis against TB
|
|
Toxicities?
|
Hemolysis if G6PD deficient, neurotoxicity, hepatotoxicitiy, drug induced SLE. INH, Injures Neurons and Hepatocytes
|
|
What vitamin prevents neurotoxicity
|
Vitamin B6 (pyridoxine)
|
|
Why are toxicities particularly important to monitor in patients taking INH?
|
INH half-lives are different in fast versus slow acetylators!
|
|
Rifampin
|
P. 296
|
|
How does it work?
|
inhibits DNA-dependent RNA polymerase
|
|
What is it used for?
|
MTB, meningococcal prophylaxis
|
|
Toxicities?
|
Minor hepatotoxicity and increases P-450
|
|
How can it be used for leprosy?
|
rifampin delays resistance to dapsone when used for leprosy
|
|
What would happen if you used rifampin alone?
|
get rapid resistance
|
|
What does it do to bodily fluids?
|
makes them red/orange in color
|
|
What are the 4 R's of Rifampin
|
RNA polymerase inhibitor, Revs up microsomal p-450, Red/Orange body fluids, Resistance is rapid
|
|
Anti-TB Drugs
|
p. 296
|
|
What are the anti-TB drugs?
|
Rifampin, Ethambutol, Streptomycin, Pyrazinamide, Isoniazid (INH) -- RESPIre
|
|
What do you use for TB prophylaxis?
|
INH
|
|
What toxicity is common to all?
|
hepatotoxicity
|
|
AUTHOR
|
Michael Shino
|
|
Resistance mechanisms for various antibiotics
|
p297
|
|
Most common resistance mechanism for penicillins / cephalosporins.
|
Beta-lactamase cleavage of beta-lactam ring.
|
|
Most common resistance mechanism for aminoglycosides.
|
Modification via acetylation, adenylation, or phosphorylation.
|
|
Most common resistance mechanism for vancomycin.
|
Terminal D-ala of cell wall component replaced with D-lac; decrease affinity.
|
|
Most common resistance mechanism for Chlorampenicol.
|
Modification via acetylation.
|
|
Most common resistance mechanism for macrolides.
|
Methylation of rRNA near erythromycin's ribosome-binding site.
|
|
Most common resistance mechanism for tetracycline.
|
Decrease uptake or increase transport out of cell.
|
|
Most common resistance mechanism for sulfonamides.
|
Altered enzyme (bacterial dihydropteroate synthetase), decrease uptake, or increase PABA synthesis.
|
|
Nonsurgical antimicrobial prophylaxis
|
p297
|
|
Drug of choice for meningococcal infection.
|
Rifampin (drug of choice), minocycline.
|
|
Drug of choice for gonorrhea.
|
Cefriaxone.
|
|
Drug of choice for syphilis.
|
Benzathine penicillin G.
|
|
Drug of choice for history of recurrent UTIs.
|
TMP-SMX.
|
|
Drug of choice for Pneumocystis carinii pneumonia.
|
TMP-SMX (drug of choice), aerosolized pentamindine.
|
|
Anti-fungal therapy
|
p297
|
|
Mechanism of action of the anti-fungal therapy polyenes.
|
Form artificial pores in the cytoplasmic membrane.
|
|
Mechanism of action of the anti-fungal therapies terbinafine and azoles.
|
Terbinafine blocks the conversion of squalene to lanosterol. Azoles block the conversion of lanosterol to ergosterol.
|
|
Mechanism of action of the anti-fungal therapy flucytosine.
|
Blocks the production of purines from the precurors.
|
|
Mechanism of action of the anti-fungal therapy griseofulvin.
|
Disrupts microtubles.
|
|
Amphotericin B
|
p298
|
|
Mechanism of action of Amphotericin B.
|
Binds ergosterol (unique to fungi); forms membrane pores that allow leakage of electrolytes and disrupt homeostasis. "Amphotericin 'tears' holes in the fungal membrane by forming pores."
|
|
Clinical uses of Amphotericin B.
|
Used for a wide spectrum of sytemic mycoses. Cryptococcus, Blastomyces, Coccidioides, Aspergillus, Histoplasma, Candida, Mucor (systemic mycoses). Intrathecally for fungal meningitis; does not cross blood-brain barrier.
|
|
Symptoms of Amphotericin B toxicity.
|
Fever/chills ("shake and bake"), hypotension, nephrotoxicity, arrhythmias ("amphoterrible").
|
|
Nystatin
|
p298
|
|
Mechanism of action of Nystatin.
|
Binds to ergosterol, disrupting fungal membranes.
|
|
Clinical use of Nystatin.
|
Swish and swallow for oral candidiasis (thrush).
|
|
Fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole, voriconazole.
|
p298
|
|
Mechanism of action for fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole, voriconazole.
|
Inhibits fungal steroid (ergosterol) synthesis.
|
|
Clinical uses of fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole, voriconazole.
|
Systemic mycoses. Fluconazole for cryptococcal meningitis in AIDS patients and candidal infections of all types (i.e., yeast infections). Ketoconazole for Blastomyces, coccidioides, Histoplasma, Candida albicans; hypercortisolism.
|
|
Symptoms of fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole, voriconazole toxicity.
|
Hormone synthesis inhibition (gynecomastia), liver dysfunction (inhibits cytochrome P-450), fever, chills.
|
|
Flucytosine
|
p298
|
|
Mechanism of action of Flucytosine.
|
Inhibits DNA synthesis byconversion to fluorouracil, which competes with uracil.
|
|
Clinical uses of Flucytosine.
|
Used in sytemic fungal infections (e.g. Candida, Cryptococcus).
|
|
Symptoms of Flucytosine toxicity.
|
Nausea, vomitting, diarrhea, bone marrow suppression.
|
|
Caspofungin
|
p298
|
|
Mechanism of action for Caspofungin.
|
Inhibits cell wall synthesis.
|
|
Clinical use of Caspofungin.
|
Invasive aepergillosis.
|
|
Symptoms of Caspofungin toxicity.
|
GI upset, flushing.
|
|
Terbinafine
|
p298
|
|
Mechanism of action of Terbinafine.
|
Inhibits the fungal enzyme squalene epoxidase.
|
|
Clinical use of Terbinafinel.
|
Used to treat dermatophytoses (especially onychomycosis).
|
|
Griseofulvin
|
p298
|
|
Mechanism of action of Griseofulvin.
|
Interfers with microtubule function; disrupts mitosis. Deposits in keratin-contianing tissues (e.g. nails).
|
|
Clinical use of Griseofulvin.
|
Oral treatment of superficial infections; inhibits growth of dermatophytes (tinea, ringworm).
|
|
Symptoms of Griseofulvin toxicity.
|
Teratogenic, carcinogenic, confusion, headaches, increase warfarin metabolism.
|
|
Antiviral chemotherapy
|
p299
|
|
Viral adsorption and penetration into the cell is blocked by ---------.
|
Gama-globulins (non-specific).
|
|
Uncoating of the virus after its penetration into the cell is blocked by --------.
|
Amantadine (influenza A).
|
|
Early viral protein synthesis is blocked by --------.
|
Fomivirsen (CMV).
|
|
Viral nuclei acid synthesis is blocked by --------.
|
Purine, pyrimidine analogs; reverse transcriptase inhibitors.
|
|
Late viral protein synthesis and processing is blocked by --------.
|
Methimazole (variola); protease inhibitors.
|
|
Packaging and assembly of new viron is blocked by --------.
|
Rifampin (vaccinia).
|
|
Amantadine
|
p299
|
|
Mechanism of action of Amantadine.
|
Blocks viral penetration/uncoating; may buffer pH of endosome. Also causes the release of dopamine from intact nerve terminals. "Amantadine blocks influenza A and rubellA and causes problems with the cerebellA."
|
|
Clinical uses of Amantadine.
|
Prophylaxis for influenza A; Parkinson's disease.
|
|
Symptoms of Amantadine toxicity.
|
Ataxia, dizziness, slurred speech. (Rimantidine is a derivative with fewer CNS side effects.)
|
|
Zanamivir
|
p299
|
|
Mechanism of action of Zanamivir.
|
Inhibits influenza neuraminidase.
|
|
Clinical use of Zanamivir.
|
Both influenza A and B.
|
|
Ribavirin
|
p299
|
|
Mechanism of action of Ribavirin.
|
Inhibits synthesis of guanine nucleotides by competitively inhibiting IMP dehydrogenase.
|
|
Clinical use of Ribavirin.
|
RSV (respiratory syncytial virus).
|
|
Symptoms of Ribavirin toxicity.
|
Hemolytic anemia. Severe teratogen.
|
|
Acyclovir
|
p299
|
|
Mechanism of aciton of Acyclovir.
|
Perferentially inhibits viral DNA polymerase when phosphorylated by viral thymidine kinase.
|
|
Clinical use of Acyclovir.
|
HSV, VZV, EBV. Mucocutaneous and genital herpes lesions. Prophylaxis in immunocompromised patients.
|
|
Symptoms of Acyclovir toxicity.
|
Delirium, tremor, nephrotoxicity.
|