1. AntiEpileptics
1.1. Treatment of seizures -Epileptiform event- a sudden excessive depolarisation of cerebral neurones which may remain localised (focal epilepsy) or spread (generalised epilepsy)
1.1.1. Carbamazepine Lamotrigine Sodium Valproate
1.1.2. With significant OAR's Vigabatrin(Perm loss of vision) Topiramate(can induce 6D myope)
2. Antipsychotics
2.1. Also called neuroleptics or makor tranquilisers. -Indicated in schizophrenia, mania and psychotic depression and may be useful for short term sadation in agression or agitation. -Have important prophylactic effect in schizphrenia -Divided into typical and atypical
2.1.1. Typical(also called conventional)-act at dopamine receptors
2.1.1.1. Phenothiazines e.g Chloropromazine Thioxanthenes e.g flupentixol Butyrophenones e.g Haloperidol
2.1.2. Atypical, act on other receptors as well as dopamine, and are less likely to cause movement disorders as a side effect than typical.
2.1.2.1. Amisulpride ClozaPINE OlanzaPINE QuetiaPINE Risperidone
2.2. Psychosis induced by increase levels of dopamine activity -Most antipsychotic drugs postsynaptic dopamine receptors (D2 in particular)
3. Anti Inflammatory Drugs
3.1. Corticosteriods
3.1.1. Glucocoticoids
3.1.1.1. Hydrocortistone
3.1.1.1.1. Regulates blood sugar levels and recovery from injur
3.1.1.2. Pharmacological Actions
3.1.1.2.1. Anti inflamtory and immunosupressive via reduction of inflammatory mediators, e.g. eicosanoids, platelet-activating factor and interleukins
3.1.1.2.2. Metabloc effect on carbohydrates, protiens and fats
3.1.2. Mineralocorticoid
3.1.2.1. Aldosterone
3.1.2.1.1. Na+ baance and reuptake, so water retention so influences blood pressure
3.1.3. ACTH regulates corticosteriod levels
3.1.4. Action
3.1.4.1. Steriod receptors bind to glucocorticoid response element in chromatin
3.1.4.1.1. DNA transcription
3.1.4.2. Site of inflammation
3.1.4.2.1. Mediators activated, endotheial activation
3.1.4.3. Elcosonoid synthesis
3.1.4.3.1. Cyclo-oxygenase
3.1.4.3.2. Phospholipase a2
3.1.5. Therapeutic uses, (systemic)
3.1.5.1. Anti inflammatory e.g ezcema
3.1.5.2. Replacement therapy disease of adrenal gland
3.1.5.3. Chemotherapy, e.g leukimia
3.1.5.4. Immunosupression e.g post transplantation
3.1.6. Adverse effect can cause diabetic mellitus, impaired glucouse tolerance Opthalmic effect: Posterior sub-capsular cataract Principal acute adverse reaction is raised IOP, can occur with topical inhaled or systemic steroids
3.1.7. Opthalmic Corticosteroids
3.1.7.1. Used in acute and chronic inflammatiom.
3.1.7.1.1. Anterior uveitis or post op .
3.1.7.2. Potenccy
3.1.7.2.1. Potency of glucocoticid steriods is not just dependent on strength but also:
3.1.7.3. Severe inflammation: Prednislone acetate and Dexamethasone
3.1.7.4. Mild: low strength prednislone sodium 0.05 or 0.1% or hydrocortistone
3.1.7.5. Available preparations
3.1.7.5.1. BetamethsONE DexamethasONE FlurometholONE < 2nd lowest iop then MedrystONE PrednislONE RimexolONE Loteprednol
3.2. NSAIDs
3.2.1. Prevent formation of Eicosanoids
3.2.1.1. Biological actions
3.2.1.1.1. Principle Eicosanoids, Leukotrines and prostaglandins
3.2.2. Indicatios
3.2.2.1. Post op
3.2.2.1.1. Corneal trauma
3.2.3. Drugs
3.2.3.1. Diclofenac sodium
3.2.3.1.1. Reduction of post op inflammaion Pain following corneal trauma Seasonal allergic conjunctivitis
3.2.3.1.2. Additional supply
3.2.3.2. Flurbiprofen Ketorolac Trometaamol Nepafenac
3.3. Anti Allergy Drugs
3.3.1. Anti Histamines
3.3.1.1. Systemic used to treat symptoms f Hayfever e.g Cetirizine, 10mg for adults 5mg child > 2
3.3.1.1.1. Topical for SAC,
3.3.1.2. AntazolINE(P) AzelastINE(POM) EpinastINE(POM) Ketotifen(POM) OlapatadINE(POM)
3.3.1.2.1. Olapatadine Ketofien Azelastine avalible on additional supply
3.3.2. Mast Cell Stabilise (7-14 days sypmtomatic relief)
3.3.2.1. Block calcium influx into mast cell membrane preventing degranulation
3.3.2.1.1. Sodium Cromoglicate (P) disadvantage 4x a day ike Lodoxamide
3.3.2.2. Nedocromil SAC, PAC. However more expensive than cromoglicate
3.3.2.3. Sodium CHrmoglicate (P,POM) Lodaxamide(P,POM) Nedocromil(POM) x2 but expensive
3.3.2.3.1. All precrible on additional supply
3.3.3. Vasoconstrictors
3.3.3.1. Stimulation of apha adrenoceptors, causing constriction of conjunctival blood vessels. Decrease in conjunctival hypermia and odema
3.3.3.2. XylometazolINE >12 years Naphazoline Phenylephrine not available in the UK
4. Antiinfectives
4.1. Antibacterial agents
4.1.1. Drugs affecting Cell wall synthesis
4.1.1.1. Penicillins, Cephalosporins
4.1.2. Bacterial cell Membrane
4.1.2.1. Polymyxin B, Propamidine
4.1.2.1.1. POlymixn B additonal suuply
4.1.3. Bacterial protien synthesis
4.1.3.1. Aminoglycosides, Tetracyclines Chloramphenicol, Fusidic acid
4.1.4. Bacterial DNA Synthesis
4.1.4.1. Fluroquinolone
4.1.5. Bacterial Metabolism
4.1.5.1. Sulphonamides
4.1.5.1.1. Interaction with local anaesthetics Tetracaine amethocaine
4.2. Anti infectives available to Optoms
4.2.1. Cloramphenicol, fusidic acid, Promamidine
4.2.1.1. Cloramphenicol 5%(P&POM), Broad, exc Pseudomonas, Good safety profile & low resistance. Drops x4 a day, 1/52 Redidrops & Chrloromycetin ointment & unit doses
4.2.1.1.1. Mode of action, binding of cholramphenicol to peptidyl transferase on the 50S ribosome prevents the new incorporation of amino acids
4.2.1.2. Fusidic acid 1%(POM). Good against +ve gram esp staph aureus. Bacterastatic(inhibit bacteria growth, and bacteriacidal in higher concentrations. Not good in Child conjuntivitis, and used 2x 1/52, Fucithalmic formulation. Used in prophylaxis of corneal abrasion and in Bleph.
4.2.1.3. Promamidine(P), is a diamidine disinfectant. Anti fungal anti ameobic. Deals with +ve gram bacteria not great with -ve. Used in acandthomeba with PHMB and minor infections such as conunctivitis and bleph. 4x day. Brolene & Golden eye oitnment
4.2.2. Independently Prescribed
4.2.2.1. Polymyxin b
4.2.2.1.1. Attaches and interferes with cell membrane of aerobic -ve gram bacteria and prevents cell way synthesis of +ve gram bacteria, POM
4.2.3. Medicines act exemptions -Provided it is in the course of their profesional practice an n a emergency optoms ca seel or supply
4.2.3.1. 0.5% cloramphenicol eye drops or 1% eye ointment -Cyclopentolate hydrocholoride -FUsidic acid Tropicamide
4.3. Quinolones
4.3.1. Inhbit DNY gyrase, broad spectrum:
4.3.1.1. -Ofloxacin, Ciprofloxacin Levofloxain, Moxifloxacin
4.4. Aminoglycosides
4.4.1. Inhibits protien synthesis. Bacteriidal. -ve gram
4.4.1.1. Epithelia toxcitiy, not used often as toxic to cornea. - Gentamycin, Tobramycin
4.5. Chlaymdia
4.5.1. Azithromycin, for trachomatous conjunctivitis caused by Chlaymdia, off license use in bleph
4.6. Aciclovir
4.6.1. Enters cell, becomes aciclovir phosphate by TK herpes enzyme. Two phosphates added becomes aciclovir triphosphate and competes with dGTP for DNA polymerase.
4.6.2. Ganciclovir
4.6.2.1. Ocular implant to treat cytomegavirus
4.7. Acanthamoeba Keratitis
4.7.1. Treat with Propamidine 0.1% and PHMB 0.02% or cholrohexidine 0.02%. Hourly for two days then reduce. PHMB and cholrohexidine work well together against cyst.
4.8. Tertracylines
4.8.1. Inhibit bacteria protien synthesis by blocking attachment of transfer RNA amino acid to the rbiosome, also used in bleph.
4.8.1.1. DoxycycLINE MinocycLINE
4.8.2. bind strongly to calcium and calcium rich foods, esp milk, preventing their absorption) -contraindictated in pregnancy and babie competes for calcium affects tooth and bone formation
5. Systemic Drugs: CNS
5.1. Prescribing in Depression
5.1.1. Moderate to severe depression, anti depressants are effective as psychological intervention.
5.1.1.1. Choice of drug depends on past experince of treatment, Px choice, side effects and in more severe depression suicide.
5.1.1.2. Depression is associated with reduced levels of the monoamines in the brain e.g 5-HT(serotonin)
5.1.2. SSRI's
5.1.2.1. Recommended as suitable first line as effective as tricyclic anti depressants (TCA's) and much safe in overdose
5.1.2.2. Restore levels of 5-HT in the synaptic cleft by binding at the 5-HT re-uptake transporter preventing the reuptake and subsequent degradation of 5HT
5.1.2.3. CitaloPRAM EscitaloPRAM FluoxeTINE(most common) ParoxeTINE
5.1.3. Tricyclic Anti Depresants
5.1.3.1. Bind to 5-HT and Nor adrenaline reuptake transporters, prevent binding and stop reuptake. Normal range of monamines build up
5.1.3.1.1. AmitriptyLINE ClomipraMINE imipraMINE LofepraMINE
5.1.4. Serotonin & Noradrenaline reuptake inhibitors
5.1.4.1. Block reuptake of these neurotransmitters, hence increasing concentration at synaptic cleft
5.1.4.1.1. Venlafaxine Duloxetine
5.1.5. MAOI's (Monoamine oxidase inhibitors)
5.1.5.1. Non selectively and irreversibly inhibit monoamine oxidase (MAO-A & MAO-B)
5.1.5.1.1. MAOI's may have role in resistant or atypical treatment, but limited use currently due to dietary restrictions (foods contating tyramine) interactions and toxcity in overdose of this group drugs
5.1.5.2. Monamine oxidase A is an enzyme involved in the metabolism of monoamines 5-HT and noradrenaline, converts monoamines into their corresponding carboxylic acid -This inhibits monoamine degradation and result in greater stores being available for release
5.1.5.2.1. Phenelzine Isocarboxazid Moclobemide
5.1.6. Lithium(and digioxin) used in depression, careful when prescribing in old people as narrow therpeutic index
5.2. Hypnotics and Anxiolytics
5.2.1. Short term management of Insomnia
5.2.1.1. Benzodiazepines, have cShort Half Life -NitrazePAM -lurazePAM Non-benzodiazepine hypnotics Zopiclone
5.2.2. Short term relief (2-4wks) of anxiety that is severe, unbearable distress. If it is mild anxiety avoid. -Chornice anxiety Px may be better with anti depressants
5.2.2.1. Benzodiazepines, long life(Anxiolytics) -DiazePAM -LorazePAM -OxazePAM
5.2.3. It is believed that benzodezepnes act by enhancing the action of GABA at GABAa receptors
5.3. Parkinsons disease
5.3.1. Involves progressive degeneration of pigmented cells in the substantia nigra leading to a deficiency of the neurotransmitter dopamine
5.3.1.1. Dopamine receptor Agonists: Bromocriptine Carbergoline Lisuride Pergolide Ropinrole Antimuscarincs: Benzatropine Orphenadrine Procyclidine
6. Dry Eye Preparations
6.1. Ocular Lubricants: Dry EYe
6.1.1. Artificial tears limitations- -Formulation cannot replace complexty of tears -Administered intermittently rather than continuously, this increases contact time (Mucoadhesive polymers) -Presence of preservatives can compromise ocular surface
6.1.2. Mild disease: -artificial tears 4x a day Moderate: -Unpreserved tears up to 12x and lubricating ointment at night -Tear conservation Severe: Immunotherapy (Ciclosporin) autologous therapy(serum) Tear conservation
6.1.2.1. Autologous serum is blood spun, tear replaced. No preservatives, has to be refigerated.
6.1.2.2. Alt therapies, omega 3 and omega 6 fatty acids
6.1.3. Formulations: Cellulose esters Carbomers Polyvinyl alcohol Sodium Hyaluronate Lubricating ointments(paraffin) Acetyle Cysteine liposomes
6.1.3.1. Cellulose ester 1.0% e.g HypromelLOSE HydroxyethlcelluLOSE MethyicelluLOSE CarboxymethylcelluLOSE
6.1.3.1.1. -Good retention time on ocular suface -Causes crusting of eyelids mimicking Bleph
6.1.3.2. Carbomers Gel tears
6.1.3.2.1. Synthetic -Good retention time on ocular surface -GOod viscousity -Tends to blur vision
6.1.3.3. Polyvinyl alchol -Synthetic -Low viscosity -Beneficial in mucin and lipid deficiency -Short retention time(good for mild , no blurry or crusting)
6.1.3.4. Sodium Hyaluronate(Blink) -Naturally occurring mucopolysaccharide -VIscous formulatons -Excellet retentoin time on ocular surface( superior to PVA and Cellulose esters) -Blurs a little
6.1.3.5. Paraffin High viscosity -Contribute to rebuild the lipid layer -Melts at temp of ocular surface -Long retention time -Useful when used with artificial tears when used at night -Blurred vision
6.2. Ocular lubricants carried on
6.2.1. CE products ocular lubricants due to easier accreditation, just have to be safe and sterile. Problem for NHS prescriptions
6.2.2. Mucoadhesive viscous gels increase contact time with the ocular surface. This causes blurring and sticky lids.
6.2.3. Tear viscosity vs blinking non-newtonian, decreases the more u blink
6.2.3.1. Tear modification
6.2.3.1.1. ilube Acetylcysteine 5-10% -Dissolves mucous filaments by breaking disulphide bonds -stinging sensation on installation into the eye
6.2.4. Preservatives
6.2.4.1. Unit does preservative free systems Increased preseervative per minim more toxcitiy/diseases
6.2.4.1.1. BAK cholride is a avidly taken up by SCL and is released slowly, exceeding upper safety limits -HWC lenses absorb more BAK then low woter content lenses -Hard CL's take up a very small amount o BAK, with a release approaching thw upper limit of safety -Tear film concentrations of BAK after instillation of eye drops with SCL could result in adverse effects of the ocular surcace
6.2.4.2. Newer opthalmic preservatives, reduce toxcitiy
6.2.4.2.1. Purite: Dissociates into water, oxygen, sodium and cholrine free radicals Sodium Perborate: Converts into water and oxygen on instillation Sofzia:Modified into harmless elements on instillation Polyquatermium Less toxic than BAK, common in multidose contact lens care products
6.2.4.3. Other multi-dose preservative free preparations
6.2.4.3.1. Hylotear 0.1% hyaluraonate Hyabak 0.15% hyaluronate Hyloforte 0.2% hyalurronate
6.2.5. Lipsomal spray
6.2.5.1. Aqueous suspension of phospholipd-containing liposomes containing hydrogenated phosphatidylcholine has been shown to be beneficial in the evaporative dry eye.
6.3. CE product, Systane
6.3.1. Systane contains hydroxypropyl (HP) guar, increases in vicosity after contacting ocular sufrace. Change is based on Ph Value, when systane placed in eye ph of 7.4 a chemical reaction occurs. HP guar binds to the ocular surface and simultaneously crosslinks with borate ions in the solution, forming a network with a gel-like consistency.
6.4. Immunosuppresants/immunimodulators
6.4.1. The pathogenesis of dry eye disease has recognised inflammation as a key pathogenetic mechanism.
6.4.1.1. Restasis(0.05% cyclosporine opthalmic emulsion)
6.4.1.1.1. Keratoconjunctivitis sicca (KCS), also called dry eye syndrome (DES
6.4.1.1.2. The first commercially avalible pharmaceutical therapeutic agent for treatment of DE.
7. Anti Glaucoma
7.1. Treatment
7.1.1. Target IOP. Prevent further glacoumatous damage
7.1.1.1. Most Px treated first with topical medication
7.1.1.1.1. Laser trabeculoplasty
7.2. Anti Glacouma Drugs
7.2.1. Licenses as IOP lowering agents, lowered by 20-35%. 5-7 mmHg on avg.
7.2.1.1. Medical therapy should start with one drug, monotherapy. Then substituted with another if non tol or not effected. Last resort is combo of drugs
7.3. Mechanism of action
7.3.1. Ideal drug: -Highy effective -Well tolerated, mim side effects -Simple to use, maximal compliance -Cost effective
7.3.2. TOPICAL DRUGs: 1.Reduce aqueous production (CA;s, a recptor agonists, and B receptor antagonist).
7.3.2.1. 2.Increase outflow through conventional trabecular meshwrk (cholinergics, bimataprost)
7.3.2.1.1. 3.Increase Uveoscleral flow (PG agonists, brimonidine)
7.3.3. SYSTEMIC DRUGS 1.Reduce aqeous production, CAI's, B receptor antagonists). Osmotic agents- dehydrate vitreous (mannitol, glycerol)
7.4. Drugs carried on
7.4.1. All drugs efficacy 1. PA 2. BA 3.Alpha 2 agonists 4. Cholinergic agonists 5. CAI's
7.4.1.1. 1.PA
7.4.1.1.1. 1st choice in OAG. -Act as prostogladin F receptors, responsive to Prostogladin f2a (PGF2a) -Increase Uveo outflow -IOP reduced within 2-4hrs, peak at 8-12hrs -One drop preferbly in the evening
7.4.1.2. Safety of drug: 1. PA 2.Cholinergic agonists 3.CAI's 4.Alpha Adrenegics 5 BA
7.4.2. PG agonist efficacy
7.4.2.1. 1.LatanoPROST 2.TravoPROST 3.BimatoPROST(dif mode of action) 4.TafluPROST
7.4.2.1.1. Timolol was gold standard until Lantanprost came along.
7.4.2.1.2. Hyperaemia: Least likely: Bimatoprost Latnoprost Travoprost Tafluprost : Mostl likely
7.4.3. Beta Receptor Antagonists
7.4.3.1. Mode of action unkown 20-40% reduction in IOP
7.4.3.1.1. Block B receptors (sympathetic) reducing aqeuous formation -selective beta blockers (B1) and non selective (B2) -Lowest concentration given to reduce side affects -Can display tachyphylaxis, reduced effectiveness over time
7.4.4. Alpha-2 recptor agonists
7.4.4.1. -Decrease aqueous production -Increacse outlow -20-30% IOP reduction - DIsplay tachphylaxis
7.4.4.1.1. -Apraclonidine Hydrochloride -Brionidine tartrate
7.4.5. CAI's
7.4.5.1. Decrease aqueous production by inhibiting enzyme involved in aqueous secretion -Topical and systemic formulations -15-20% reduction in IOP -Oral formulation used in the treatment of acute angle closure
7.4.5.1.1. Carbonic anhydrase catalyse's HC03 transporting aqueous
7.4.5.1.2. BrinzolaMIDE DorzoloMIDE Oral AcetazolaMIDE
7.4.5.2. Side effects: Topical: Polyuria blurred vision flashes Oral, sysemic: Allergy Depression
7.4.6. Cholinergic Agonists
7.4.6.1. -Parasympathomimetics -Pharmocological action: Increase aqueous outflow -Open trabecular meshwork, increase outflow
7.4.6.1.1. Pilocarpine 0.1-6%(very commonly used) Pilogel
7.4.6.2. SIde effects
7.4.6.2.1. -Miosis -Myopia -Retinal Detachment
7.4.7. Combination drugs
7.4.7.1. Timolol + A RANGE
7.4.8. Compliance
7.4.8.1. -Simplicity of treatment -Memory -Understanding of disease -side effects
7.4.8.1.1. GUidelines: -One drugs regardless of IOP -Show how to put drops in -Check IOP in 3/12
7.4.8.2. If prescribing Beta antogonissts Asl about inhalers -Check peak flow, pulse -COnsider drug interactions
8. Systemic Drugs: Cardiovascular
8.1. Cardiovascular DIsease
8.1.1. Angina and MI and cerbrovascular disease (stroke), amonst highers causes of deaths -CV diseases have risk factors -Non modifiable -age, gender, and family history -Modifible - Smoking, hyperension and hyperlipidaemia
8.1.1.1. Modifiable- -Lifestyle changes Other require pharmological interventons: HYpertension(drugs to lower BP) Lipid modification
8.1.2. DIagnosing Hypertension: -140/90 or higher, monitor. -White coat hypertension is a worried PX heart rate high for no reason -180/110- Malignant hypertension, could be papiloedema
8.1.2.1. AIm of treatment: Reduce diastlolic BP to <=90mmhG(resting) Reduce systolic BP to <=140mmHg
8.2. How to we treat Hypertension
8.2.1. -Stepped approach -Low doeses of "several drugs" (minimising adverse events and maximises PX compliance
8.2.2. 1st line of treatment ACE inhibitors
8.2.2.1. -Competititively inhibit agiotensin converting enzyme ACE -Ace converts angiotensin 1 to active angiotensin 2 -Angiotensin 2 i s a potent vasoconstrictor
8.2.2.1.1. CaptoPRIL EnalaPRIL LisinoPRIL RamiPRIL
8.2.3. Angiotensin 2 receptor antagonists
8.2.3.1. -Inhibit receptor at which Angiotensin 2 acts, fewer side affects than ACE inhibitors
8.2.3.1.1. CandersarTAN LosarTAN ValsaTAN
8.2.4. Calcium Channel Blockers
8.2.4.1. CCB's inhibit all inward movement o calcium ions through slow L type calcium channels in active memebranes such as: -Cells of the myocardium -Cells within the His-purkinje system of the heart -Cells of vascular smooth muscle -Affects cardiac contractility and causes vasodilation
8.2.4.1.1. -Causes vasodilation of arteries and also reduce cardiac output -Useful in treatment of angina and hypertension
8.2.5. Diuretics
8.2.5.1. Promote the excretion of water -they act at different sites within the nephron and in different ways -Three classes
8.2.5.1.1. Thiazides
8.2.5.1.2. Loop Diuretics
8.2.5.1.3. Potassium Sparing
8.2.6. Beta Blockers
8.2.6.1. Perform less well than others in Hypertensions -Used in treatment for angina -Increased chance of sdie effects
8.2.6.1.1. AtenoLOL MetoproLOL
8.2.6.2. Mechanism of action could involve: -Reduction of heart rate and force of contraction -Reduction in peripheral resistance -Inhibition of renin release -Central actions to reduce sympathetic activity
8.3. Other cardiovascular disease
8.3.1. Ischaemic Heart Disease: Angina pectoris
8.3.1.1. Intermittent chest pain due to stress or exertion
8.3.1.1.1. -Caused by insufficent 02 supplied to cardiac muscle, narrowing of coronary artieries
8.3.2. Myocardial infarction(heart attacked)
8.3.2.1. ST eleveation on ECG
8.3.2.1.1. Immediate: Analgesia, Thrombolysis(move thrombosis), Aspirin Prophylaxis: Cocktal of drugs to stop future heart attacks Beta blockers ACE Inhibitors Asprin lipid loweing therapy
8.3.3. Cardiac Arrhythmias
8.3.3.1. Drug therapy indicated in Supraventricular tachycardia e.g Adenosine, Verpamil
8.3.3.2. Arrhythmias caused by wolf-parkinson-white syndrome e.g Amiodarone , Disopyramide, Flecainide
8.3.3.3. Results in change of cardiac action potential
8.3.3.4. Atrial Fibrillation e.g Digoxin, DIsopyramide, Amiodarone
8.3.3.5. Ventricular Tachycardia e.g Lidocaine, Amiodarone
8.4. Lipid Modification
8.4.1. Cholesterol and triglycerides are transported in the blood from the liver in association with lipoprotiens
8.4.1.1. LDL cholesterol associated with atheroma and cardiovascular disease
8.4.1.1.1. Lower LDL by 1mmol reduced CVD events
8.5. Statins
8.5.1. Increase uptake of LDL from the blood, reducing cholestrol
8.5.1.1. SimvaSTATIN AtrovaSTATIN PravaSTATIN