PHARMACOLOGICAL MANAGEMENT OF THE MUSCULOSKELETAL

A.) BIPHOSPHONATES
MOA: Inhibit osteoclastic bone resorption

C.) TUMOR NECROSIS FACTOR BLOCKER

MOA: Stimulates macrophages to produce

cytotoxic metabolites, thereby increasing phagocytic killing activity.

golimumab ( Simponi) infliximab (Remicade) certolizumab pegol (Cimzia)

via a mechanism that differs from that of other antiresorptive agents [2-4]. Bisphosphonates attach to hydroxyapatite binding sites on bony surfaces, especially surfaces undergoing active resorption.
ibandronate sodium (Boniva) zoledronic acid (Reclast) tiludronate (Skelid) alendronate (Fosamax)

D.) OSTEOPOROSIS DRUGS

MOA: Inhibits the receptor activator of

nuclear factor ligand (RANKL), a cytokine that is essential for the formation, function, and survival of osteoclasts. This inhibition stops the maturation of
osteoclasts and reduces bone resorption. denosumab: (Xgeva) teriparatide (Forteo)

B.)

NONSTEROIDAL

ANTIDRUGS

INFLAMMATORY (NSAIDS)

E.) OTHERS
hormone receptor antagonist: pegvisomant (Somavert) growth hormone: somatropin (Genotropin) anti-gout drugs: colchicines (Colcrys) sphingosine 1-phosphate receptor modulator: fingolimod (Gilenya) selective serotonin and norepinephrine reuptake inhibitor: milnacipran (Savella) anticoagulant: enoxaparin sodium (Lovenox) Clostridium botulinum type - A neurotoxin complex: incobotulinumtoxinA (Xeomin) calcitonin : calcitonin-salmon (Miacalcin Nasal Spray) alpha-L-iduronidase enzyme therapy: laronidase (Aldurazyme)

MOA: Unknown. An NSAID thought to

inhibit the action of cyclooxygenase, an enzyme synthesis miosis.

etodolac (Lodine XL) rofecoxib ( Vioxx ) naproxen sodium ( Naprelan) meloxicam (Mobic) naproxen + esomeprazole (Vimovo ) abatacept ( Orencia) diclofenac sodium ( Pennsaid)

responsible

for

prostaglandin mediate the

prostaglandins

inflammatory responses and also cause

C.) ANALGESICS
MOA: Act by blocking generation of pain

F.) OTHERS
potassium channel blocker: Dalfampridine (Ampyra) Interferon Beta 1-A (Avonex) alpha2-adrenergic agonist: clonidine hydrochloride (Kapvay) sedatives: midazolam HCI VERSED monoamine tetrabenazine Xenazine H1 Silenor inhibitor mild of to acetylcholine the central system : receptors : glycopyrrolate Cuvposa stimulant nervous receptor antagonist, doxepin tricyclic antidepressants: depletory:

impulses,

probably

by

inhibiting

prostaglandin synthesis in the CNS or the synthesis or action of other substances that sensitizies pain like opoid receptors.
acetaminophen (Tylenol) capsaicin (Qutenza)

Narcotic and opiod analgesic morphine sulfate (Embeda naltrexone hydrochloride (Trexan) fentanyl buccal (Onsolis) tramadol (Ultram)

dexmethylphenidate Focalin

D.) NONSTEROIDAL ANTIINFLAMMATORY DRUGS

MOA: Unknown. An NSAID thought to

OTHERS (Cont)
nonbenzodiazepine hypnotic agent: eszopiclone Lunesta NMDA receptor antagonist: memantine HCl Namenda Eugeroics: armodafinil Nuvigil Neurodegenerative Disease Drugs: galantamine hydrobromide Reminyl selective, activated radiopaque antipsychotic paliperidone Invega irreversible GABA enzyme-

inhibit the action of cyclooxygenase, an enzyme responsible for prostaglandin synthesis prostaglandins mediate the inflammatory responses and also cause miosis.
diclofenac potassium (Zipsor) ketorolac tromethamine (Sprix)

E.)

PHOSPHODIESTERASE

transaminase agents: medication:

(PDE5) INHIBITOR
MOA: Block the degradative action of phosphodiesterase type 5 on cyclic GMP in the smooth muscle cells lining the blood vessels vardenafil (Levitra) tadalafil (Cialis)

inhibitor: vigabatrin Sabril contrast odixanol Visipaque

b.) PENICILLIN
MOA: An aminopenicillin that prevents

bacterial replication.

cell-wall

synthesis

during

PHARMACOLOGICAL MANAGEMENT OF THE NEUROLOGIC SYSTEM

amoxicillin (Amoxil) amoxicillin and clavulanate potassium (Augmentin)

A.) CORTICOSTEROIDS
MOA:

Decreases and/or

the

inflammatory immune

C.) SULFONAMIDES
MOA: It inhibits formation of dihydrofolic

responses

suppresses

response of the brain giving then relief to any hematomas brought about the inflammation.
glatiramer (Copaxone) natalizumab (Tysabri) difluprednate (Durezol)

acid from PABA, also inhibits dihydrofolate reductase formation. Both decrease bacterial folic acid syntheses bactericidal.
sulfamethoxazole trimethoprim (Bactrim) acetyl sulfisoxazole (Gantrisin) and

D.) CEPHALOSPORIN
MOA:

B.) ANTICONVULSANTS
MOA:

It inhibits cell wall synthesis, osmotic instability, usually

Unkown.

Thought

to

stabilize

promoting

neuronal membranes and limit seizure activity by either increasing efflux or decreasing influx of sodium ions across cell membranes in the motor cortex during generation of nerve impulses

bactericidal. It also promotes osmotic instability.

cefuroxime (Ceftin) cefprozil (Cefzil) cefpodoxime (Vantin) cefixime (Suprax) oracarbef (Lorabid) cefaclor (Raniclor)

Rufinamide ( Banzel) clonazepam (Klonopin) divalproex sodium (Depakote) pregabalin (Lyrica) carbamazepine (Tegretol) lacosamide (Vimpat) gabapentin (Neurontin) topiramate (Topamax)

E.) ANTIVIRALS
MOA: inhibits of binding deoxyguanosine

G.) ANTIHISTAMINE
MOA: Acts in the reduction of histamine,

triphosphate to DNA polymerase, resulting in inhibition of DNA synthesis.

serotonine and other mast cell mediators release, and simultaneous selective blocking of the H1-receptors. As a result of the

trifluridine (Viroptic) idoxuridine (Herplex Liquifilm) acyclovir (Avirax) vidarabine (Flexyx) ganciclovir (Cytovene- IV) phosphonoformic acid (Foscarnet)

latter effects the level of the cell cAMP in enhanced and eosinophilic infiltration is inhibited.
ketotifen (Zaditor) patanol ()Olopatadine) levocabastine (Livostin) antolozine epinastine HCl (Elestat)

F.) MYDRIATICS
MOA: A potent mydriatic and cyclopegic

PHARMACOLOGICAL MANAGEMENT OF THE EARS

A.) MACROLIDE ANTIBIOTICS
MOA: Binding irreversibly to the 50S

whose anticholinergic action leaves the pupil under unopposed adrenergic influence, causing it to dilate.
atropine sulfate (Atropisol) cyclopentolate hydrochloride (Cyclogyl) epinephrine hydrovhloride (Glaucon) epinephryl borate (Epinal) homatropine hydrobromide (Homatropine) phenylephrine hydrochloride (Prefrin) scopolamine hydrobromide (Ispto Hyoscine)

subunit of bacterial ribosomes and by binding to the ribosome, macrolides inhibit translocation during translation This bacteriostatic, of action that is meaning tRNA mainly bacterial

growth and reproduction are inhibited, in contrast to bactericidal antibiotics which directly kill bacteria.
erythromycin (Pediazole) azithromycin (Zithromax) clarithromycin (Biaxin) dirithromycin (Dynabac)

Pharmacological management of the eyes

A.) CORTICOSTEROIDS
MOA: Decreases inflammatory, mainly by

C.) MAST CELL STABILIZERS

MOA: Block a calcium channel essential

for mast cell degranulation, stabilizing the cell and thereby preventing the release of histamine and related mediators. One suspected pharmacodynamic mechanism is the blocking of IgE-regulated calcium channels. Without intracellular calcium, the histamine vesicles cannot fuse to the cell membrane and degranulate.
nedocromil sodium (Alocril) cromal (Cromolyn) ketotifen (Zaditor) pemirolast potassium (Alamast) olopatadine (Pataday)

stabilizing

leukocytye

lysosomal

membranes; suppresses immune response; stimulates bone marrow; and influences protein, fat and carbohydrate metabolism
flomex (Fluorometholone, FML) loteflam (Loteprednol etabonate) pred forte (Prednisone acetate)

B.)

NONSTEROIDAL

ANTIDRUGS

D.) ANTIBIOTICS
MOA: inhibits bacterial cell-wall synthesis

INFLAMMATORY (NSAIDS)

MOA: Unknown. An NSAID thought to

; may be bactericidal or bacteriostatic, depending on concentration and infection.

cipmox (Ciprofloxacin) gentamicin (Garamycin) garamycin( (Ofloxacin) tobrex (Tobramycin) vigamox (Monofloxacin) erythromycin (Erycette)

inhibit the action of cyclooxygenase, an enzyme synthesis responsible for prostaglandin mediate the

prostaglandins

inflammatory responses and also cause miosis.

acular (Ketorolac) nepafenac (Nevanac) flurbiprofwen sodium (Ocufen) xibrom (bromfenac)