ANTIVIRAL: Virus: Mechanism: + - Notes:

Acyclovir HSV- -->Monophosphate (by viral 1. Inhibits DNA -Very poorly absorbed -Anti-herpes nucleoside
1, enzymes) --> Diphosphate (by Synthesis -Multiple times a day. analog.
HSV-2 host kinases) --> Triphosphate '-- 2. Chain -SE: GI and HA -Topical for local reactivatio
> 1. Competetive inhibition of Termination (common), renal and -Oral & IV for initial,
DNA polymerase --> inhibition of neural (uncommon) recurrent, suppression
DNA synthesis. 2. Incorporation -Drug interactions, no
into viral DNA --> Chain use with other
Termination nephrotoxics.
Ganciclovir CMV Same as Acyclovir Same as Acyclovir
CCR5 Inhibitors HIV Competitive inhibitor of CCR5, which is -Substrate of CYP3A4, -Entry inhibitor (Fusion)
the CD4 coreceptor that HIV binds. many drug -Used to bridge, not seen
interactions much anymore.
Zidovudine HIV Reverse transcriptase inhibitor SE: Lactic acidosis, Nucleoside (NRTI)
Chain terminators Peripheral fat wasting, Similar to Acyclovir
bone marrow
suppression (oral
ulcers), nausea, facial
lipoatrophy.
Efavirenz HIV Direct binding to RT enzyme SE: Rash, increases Non-nucleoside (NNRTI)
transaminases, CNS
(drowsiness, vivid
dreams)
Can inhibit OR induce
P450, drug
interactions
Integrase Inhibitor HIV Affects integration
Lopinavir/Ritonavir HIV Protease Inhibitor Ritonavir given SE: GI, body fat -Huge for drug interactions
Bind protease, inhibits photolytic with Lopinavir to abnormalities, -ALL inhibit P450 (but
cleavage of viral proteins, so inhibits inhibit it’s perioral paresthesias, metabolized by P450, so
activation, cleavage and viral assembly. metabolism and taste abnormalities, prolong own half life)
BONE DRUGS:
ANTIBACTERIAL:
CANCER DRUGS: Class:
Class:
Bacteria: Mechanism:
Mechanism:
Mechanism: + + -- - Notes:
Notes:Notes:
Methotrexate
Estrogen Antimetabolites Anti-Resorptive
-Competetively -Dental: decrease -SE: Hypercoagulation,
-SE: Oral mucositis, -Cell Cycle Specific
Penicillin VK, (interfere
Penicillin:with (Decrease
CWSI
inhibits bone
DHFR tooth loss, Poor
breast
absorption
cancer,
leukopenia,cholestasis
withnausea,
PO -Beta-lactam
-Other
amoxicillin DNA
Gramsynthesis
+N resorption)
(dihydrofolate
1. Inhibit increase -Shorter
(no bilethrombocytopenia,
half
flow)
life than most bone -Oral:antimetabolites
60-75%
(Penicillins) during
Amoxicillin:
S phase) reductase, cell
Penacilin cycle mandibular bone antimicrobials
-Black box
marrowwarningtoxicity,
for CVvery bioavailability,
block thymidylate
4-6
Gram +N, enzyme) binding density, decrease -Penicillin
diseasesensitive
SE: to UV and hourssynthase
to work.(another
Gram –N -Antimetabolite,
proteins gingival bleeding. Hypersensitivity
sunlight (must(mostwear -Kidney enzyme
excretion
in cell
Raloxifene Selective mimics
-Anti-Resorptive
no allow
common,
-SE: for lower
sunglasses)
anaphylaxis
Hypercoagulation, dry mouth.
rare, -Prophy:
cycle)
-Approved 1.
forAmoxicillin
estrogen Tetrahydrofolate
(Decrease bone
peptoglycan but dose
hot (Boosting)
cross-reactivity
-Resistance:
flashes. with decreasedprevention/treatment
2g PO-Works on S phase.
Lamivudine receptor HBV resorption) doesn’t
NRTI layer function like cephalosporins).
transport,
Well tolerated side Other:
increased -Augmentin:
-Hepatic
Resistance can metabolism
modulator -Binds leakage
it. estrogen Phlebitis,
effects export,
GI, Hematologic,
altered affinity
develop Amoxicillin
-Fecally + Clavulanic
excreted
over time
Ribavirin/Pegylated HCV receptor,
-Directagonist
and
effect cellin Electrolyte
Rapidlyfor disturbances,
DHFR, gene CI: Pregnancy,
absorbed, acid severe
-Ellimination half-life:
Proteins
interferon bone and lipid
-Effect death
on host (liver),
factors Neurologic, amplification
very long Renal.
half life of heart DHFR.disease,
32.5 hours. Eliminated renally
antagonist
-Immune in breast
2. Cellsystem
Lysis: effects - Amoxicillin
-Oral SE:
complications
GI -Oral
hemolytic anemia,
Cefazolin
Etoposide DNA
Gramtopological
+B and uterus.
-DNA Osmotic
topoisomerase -Succesfull in -SE: Well-SE: tolerated
Secondary leukemia.
insomnia.-IV for
-Cell
severe
Cycleinfection,
Specific
(1st gen
Calcitonin inhibitor
Gram –N II resolves
-Anti-Resorptive
pressuretopological
or treating
-Onset: 15-30 monocytic
(otherwise -Oral
same
-SE: Rhinitis, complications
GI as PO for
upset, itch -Approved -Natural,
mild/moderate
derived
for treatment
Cephalosporin) problems,
(Decrease boneEtoposide
activation of mins. leukemia, smallPenicillins
cell above) 5 -Penicillin
yearsfrom
pastplant.
like
menopause.
2nd gen Gram +N inhibits
resorption) it.
endogenous lung
-Duration: cancer,
8-24 -Resistance: all 3 ways- 1. distribution
-Works
-Subcutaneous, on G2
Cephalosporins Gram –B -Blocks
-Binds cell cycle in hours
CT autolysins.
receptors testicular cancer.
Inactivation by Penicillinase, intranasal. -Renalphase
excretion
late S phase
Cephamycin: on osteoclasts through
and cephalosporinase or ESBLs,
Anaerobes G2 phase.
kidney 2. Alterations in membrane
Vincristine
Ceftriaxone
Bisphosphonates Mitotic-blocking
Gram +N -To move,
-Anti-Resorptive -Long half life in permeability
-Poorly-Oral orcomplications
absorbed efflux (drug -Most -Cell
orally commonCycleused
Specific
for
rd
(3 gen alkaloid
Gram –B microtubules
(Decrease bone bone (10 years) can’t reach target),
(empty stomach) 3. -Works on M
osteoporosis
Cephalosporin) polymerize on one -Improves
resorption) Alterations in PBP (target
-SE: Hypocalcemia, phasefor
-Approved
4th gen Gram +B endhydroxyapetite,
-Binds and depolymerize periodontal site)
esophagitis, jaw prevention and
cephalosporins Gram –B on the
released byother. health. osteonecrosis, bone/joint treatment.
Vincristine
osteoclasts. inhibits pain, atrial fibrillation.
Carbapenems Broad polymerization.
-Interferes with -Broad SE: Hypersensitivity, -Beta-lactam
spectrum -Causes pathway.
mevalonate mitotic arrest. spectrum (Gram Seizures -Last line for resistant
Doxorubicin
Teriparatide Intercalating
Parathyroid -Slide (increase
-Anabolic between and -Protects
+, Gram -, against -Daily -Generates
subcutaneous oxygen -Cell for
-Approved
organisms. Cycle Non-
treatment
antibiotic
hormone bonebind stacked DNA periodontitis-
formation) Anaerobes) radicals that lead to of-IV
-SE: Hypercalcemia, highSpecific
onlrisk
bases
-Binds PTH-1(intercalation),associated
-Good bone headache,cardiotoxicity
leg cramping. -Peak 30 mins,
-Renally gone 3
excreted
-Blockon
reseptors replication and loss.
Distribution -Blackbox-Oral complications
warning for hours.
Clavulanic acid transcription
osteoblasts
Contains to
penicillins, Prevents osteosarcoma in rats.
Cyclophosphamid
(beta lactamase Alkyating agent stimulate
-Converted
binds andbone to active destruction
inhibits -Wide utility
and in -Liver produces inactive -Cell Cycle Non-
einhibitor) formation.
form in liver by P450enhances
beta-lactamase chemotherapy. metabolites (implications Specific, but most
Denosumab Antibody -Alkylation
-Monoclonal produces-Maximum
antibody -Minimal
spectrum oral -AE: hypocalcemia,
ofbone for liver tumor therapy)
severe effective
-Approved in G1 and
for treatment
antagonist of bindsmillions
RANKL.of corsslinksresorption complications
parent drug -SE:
infection, Nausea, vomiting,of highSrisk.
dermatologic phase.
Vancomycin RANKL
Gram + in DNA,
CWSI at earlier site suppression
-Works on at 1 -Too reaction,
largeboneONJ
to marrow
affect Gram – -Nitrogenevery 6
-Subcutaneous
-For beta-lactam
MRSA overwhelming
than PCN the month.
MRSA -Poor oral suppression,
absorption sterility, months. Mustards
resistant, or persons
repair mechanism. -Not affected by -SE: Infusion
-Bacteriacidal acuterelated
leukemia.(so give can’t tolerate beta-
-Forces cell to kill renal -Time slow), hypersensitivity, lactams.
itself. impairement.
dependent hematologic, ototoxicity/ -2nd line for C. difficile
Tamoxifen
Fluoride Hormonal -Reduces mitogenic
-Accumulates in bone -Prolongs
-Rapidly
killing and survival -Excess-Requires
nephrotoxicit (>1ppm) removal
leads to of -Indication:
-Cell
colitis Cycle
(only Non-
prevention
time taken
antagonist signal transduction incompletely
and teeth. -Goodafter surgery for mottling endogenous
of enamel, estrogen
brown of by Specific
dental
PO) caries.
breasteffect
-Anabolic tissue. on breastorally.
absorbed
distribution cancer in post-
staining.either natural -Renally-For breast
excreted.
-VISA/VRSA: cancer,
resistant.
-Estrogen
trabecular bone Receptor -Remineralizes
menopausal
(but poor CSF) women -SE: menopause,
Nausea, vomiting, drugs,
GI or used in