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Glossary of USMLE 1 Pharm

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amount of drug in body/_______ = Vd
plasma drug concentration

(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
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
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 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
A drug 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
In a dose response curve, a competitive antagonist shifts the curve _____, while a non-competitive antagonist shifts the curve ______.
right, down
What pharmacologic relationship would determine the existence of spare receptors?
EC50 is lower then Kd
(EC50 is more to the left)
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.
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 have the same mechanism of action as penicillin?
(3)
- Cephalosporins
- Imipenem
- Aztreonam
Bacitracin, vancomycin and cycloserine block the synthesis of this molecule, preventing cell wall synthesis
peptidoglycans
These drugs block the 50s ribosomal subunit
(4)
clindamycin
"buy at 30 CELL @ 50"
- Chloramphenicol
- Erythromycin
- Linezolid
- cLindamycin
These drugs block the 30s ribosomal subunit
(2)
"buy AT 30, cell @ 50"
- Aminoglycosides
- Tetracyclines
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
(3)
FAN the fungal cell:
- Fluconazole/azoles
- Amphotericin B
- Nystatin
What is the mechanism of action of Pentamidine
Unknown
Which is the IV form and which is the oral form of Penicillin?
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, and dicloxacillin are used mainly for what type of infection?
Staphlococcal infection (hence very narrow spectrum)
T or F: Methicillin, nafcillin, and dicloxacillin have the same mechanism of action as penicillin
TRUE
Are Methicillin, nafcillin, and dicloxacillin penicillinase resistant? If so why?
Bulkier R group makes these drugs resistant to penicillinase
What should you watch out for when giving Methicillin, nafcillin, or dicloxacillin?
Hypersensitivity rxn (urticaria,severe pruritus); methicillin can cuase interstitial nephritis
T or F: Ampicillin/amoxicillin have the same mechanism of action as penicillin
TRUE
Which has greater oral bioavailability: Ampicillin or Amoxicillin?
amOxicillin (O for Oral)
What do you use Ampicillin/amoxicillin for?
Ampicillin/amoxicillin HELPS to kill enterococci (H. influenzae, E. coli, Listeria monocytogenes, Proteus mirabilis, Salmonella)
Can penicillinase effect Ampicillin/amoxicillin efficacy?
Yes, they are penicillinase sensitive
since Ampicillin/amoxicillin are penicillinase sensitive, what inhibitor is used w/ them?
clavulanic acid
What should you watch out for when giving Ampicillin/amoxicillin?
(2)
Hypersensitivity rxn
(ampicillin rash)

Pseudomembranous colitis
Why are Carbenicillin, piperacillin, and ticarcillin 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 Carbenicillin, piperacillin, and ticarcillin?
Hypersensitivity rxn
Why does concomitant administration with clavulanic acid increase the efficacy of piperacillin and ticarcillin?
Because they are penicillinase sensitive
What is the mechanism of action of Cephalosporins?
inhibit cell wall synthesis
How are Cephalosporins 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 Cephalosporins cover what bugs?
gram positives (staph and strep) though less,
H. influenzae,
Enterobacter aerogenes, Neisseria,
Proteus mirabilis,
E. coli,
Klebsiella
(HEN PEcK)
What can 3rd generation Cephalosporin drugs do that 1st and 2nd generation can't?
Cross the blood brain barrier
What are some other benefits of 3rd gen Cephalosporins?
better activity against gram neg bugs;
resistant to beta-lactam drugs;

Ceftazidime for Pseudomonas;
Ceftriaxone for N. gonorrhea
What are the benefits of 4th gen Cephalosporins (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)
When would you use aztreonam?
(3)
Only to treat:
Klebsiella,
Pseudomonas,
Serratia spp.
Is Aztreonam 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 Aztreonam good for?
The PCN-allergic patient that can't take aminoglycosides b/c of renal insufficiency
Are there any toxicity issues with Aztreonam?
Not really. Generally well tolerated with occasional GI upset. Vertigo, Headache and rare hepatotoxicity have been reported.
What is imipenem?
broad spectrum beta-lactamase-resistant abx
What do you always administer Imipenem with and why?
cilastatin -- it decreases inactivation of imipenem in renal tubules
What do you use Imipenem for?
Gram pos cocci, gram neg rods and anaerobes (broad spectrum)
What bug is Imipenem the drug of choice for?
Enterobacter
What are its side-effects of Imipenem?
GI distress,
skin rash,
seizures at high conc.
Is Vancomycin 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 Vancomycin 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 Vancomycin?
Red man's syndrome.
Diffuse flushing which can be controlled by pretreatment with anti-histamines and with slow infusion rate
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 and damikacin)

T = Tetracyclines
What does CELL stand for?
C = Chloramphenicol,
E= Erythromycin,
L= Lincomycin,
L= cLindamycin
Which of the protein synthesis inhibitors are bactericidal?
Only the aminoglycosides are, the rest are bacteriostatic
Name some aminoglycosides?
Gentamicin, neomycin, amikacin, tobramycin and streptomycin
How do Aminoglycosides work?
They inhibit formation of the initiation complex in mRNA translation
Why are Aminoglycosides 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 the Aminoglycosides class is commonly used for bowel surgery?
Neomycin
What are the two major Aminoglycoside toxicities?
Nephrotoxicity (esp. when used with cephalosporins) and Ototoxicity (esp. when used with loop diuretics). amiNOglycosides
Name some tetracylcines
Tetracycline, doxycycline, demeclocycline, minocycline
How do Tetracyclines work?
Blocks t-RNA attachment to 30S subunit
Which tetracycline can you use in patients with renal failure and why?
Doxycycline

because its elimination is fecal
What drug class should you not take with a glass of milk?
Tetracyclines
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 of Tetracyclines?
(4)
Teeth discoloration,

inhibition of bone growth in children;

Fanconi's syndrome;

photosensitivity
Name (3) macrolides?
Erythromycin,

Azithromycin,

Clarithromycin
How do Macrolides work?
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?
(4)*
Eryc's Nipple is at his Mid Clavicular Line:

Erythromycin tx:
Neisseria,
Mycoplasm,
Chlamydia,
Legionella
What are the major toxicities of Macrolides?
(4)*
Macros make you GASE:

GI discomfort,

Acute cholestatic hepatitis,

Skin rashes,

Eosinophilia
What is the most common cause for non-compliance to macrolides?
GI discomfort
How does Chloramphenicol work?
inhibits 50S peptidyltransferase
Main use of Chloramphenicol?
Meningitis
(H. influenzae, N. meningitides, S. pneumo)

Used conservatively b/c of toxicity
What are the main toxicities of Chloramphenicol?
Anemia and aplastic anemia
(both dose dependent),

Gray baby syndrome
(in premes b/c they lack UDP-glucoronyl transferase)
How does Clindamycin work?
blocks peptide bond formation at 50S
When do you use Clindamycin?
Anaerobic infections

(e.g. Bacteroides fragilis and C. Perfringens)
Toxicities of Clindamycin?
(3)
Pseudomembranous colitis,

fever,

diarrhea
MC sulfonamide
Sulfamethoxazole (SMX)
How do Sulfonamides work?
Inhibits bacterial folic acid synthesis from PABA

(by blocking dihydropteroate synthase)
What are its uses?
(4)
Gram-positive,
Gram-negative,
Nocardia,
Chlamydia

(simple UTIs)
Toxicities of Sulfonamides?
(5)
hypersensitivity rxn,

hemolysis if G6PD deficient,

nephorotoxicity
(tubulointerstitial nephritis),

kernicterus in infants,

displaces other drugs from albumin (e.g. warfarin)
How does Trimethoprim work?
inhibits folic acid pathway by blocking dihydrofolate reductase
What are Trimethoprim's uses?
(4)
used in combo with Sulfamethoxazole (TMP-SMX) for recurrent UTIs,

Shigella,

Salmonella,

prophylaxis for PCP in AIDS patients
Toxicities of Trimethoprim?
(2)
Megaloblastic anemia,

Pancytopenia

(may be alleviated with supplemental folic acid)
What the most famous floroquinolone?
Ciprfloxacin (treatment for Anthrax)
How do Fluoroquinolones work?
inhibits DNA gyrase (topoisomerase II)
What are Fluoroquinolones uses?
(3)
Gram neg,

First line for Pseudomonas UTI,

Neisseria
What population is contraindicated for Fluoroquinolone use?
(2)
pregnancy and children
What are Fluoroquinolone toxicities?
(2)
FluoroquinoLONES hurt attachment to BONES:

Cartilage damage;

Tendonitis and tendon rupture in adults
How does Metronidazole work?
forms toxic metabolites in the bacteria

(Bactericidal)
What are Metronidazole uses?
(6)
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 of Metronidazole?
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

Anaerobes below diaphram:
Metronidazole
How do Polymyxins work?
disrupts osmotic properties of bacteria, acts like a detergent
What are Polymyxins used for?
resistant gram negative infections
Toxicities of Polymyxins?
(2)
Neurotoxicity,

ATN
Isoniazid
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
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 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
arachadonic acid products
pg 150
name the enzyme that liberates AA from the cell membrane
phospholipase A2
what does the lipoxygenase pathway yield
leukotrienes (L for Lipoxygenase and Leukotrienes)
LTB4 is a____
neutrophil chemotactic agent
which leukotrienes are involved in bronchoconstriction, vasoconstriction, smooth muscle contraction, and increased vascular permeability
LT C4, D4, E4 (SRS-A)
what are the 3 products of the cyclooxygenase pathway?
thromboxane, prostacyclin, prostaglandin
what are the 2 functions of TxA2
platelet aggregation, vasoconstricion
what are the 2 functions of PGI2
inhibition of platelet aggregation; vasodilation (Platelet Gathering Inhibitor)
microtubule
pg 150
what are the shape and dimensions of a microtubule?
cylindrical, 24 nm in diameter, variable length.
what are the components of a microtubule
polymerized dimers of alpha and beta tubulin (+2 GTPs per dimer)
where are microtubules found
cilia, flagella, mitotic spindles, neuronal axons (slow axoplasmic transport)
antihelminthic drug that acts on microtubules
mebendazole/thiabendazole
anti breast cancer drug that acts on microtubules (prevent disassembly)
taxol
antifungal drug that acts on microtubules
griseofluvin
anti cancer drug that acts on microtubules (prevent assembly)
vincristine/vinblastine
anti gout drug that acts on microtubules
cholchicine
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.
Ganciclovir (DHPG dihydroxy-2-propoxymethyl guanine)
p300
Mechanism of action of Ganciclovir.
Phosphorlation by viral kinase; perferentially inhibits CMV DNA polymerase.
Clinical use of Ganciclovir.
CMV, especially in immunocompromised patients.
Symptoms of Ganciclovir toxicity.
Leukopenia, neutropenia, thrombocytopenia, renal toxicity. More toxic to host enzymes than acyclovir.
Foscarnet
p300
Mechanism of action of Foscarnet.
Viral DNA polymerase inhibitor that binds to the pyrophophate binding site of the enzyme. Does not require activation by viral kinase. "FOScarnet = pyroFOSphate analog."
Clinical use of Foscarnet.
CMV retinitis in immunocompromised patients when ganciclovir fails.
Symptoms of Foscarnet toxicity.
Nephrotoxicity.
HIV therapy
p300
Saquinavir, ritonavir, indinavir, nelfinavir, amprenavir are example of this type of anti-HIV drug.
Protease inhibitor.

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