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Dr. Faizur Rahman Professor of Ophthalmolgy Peshawar Medical College Peshawar.

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Presentation on theme: "Dr. Faizur Rahman Professor of Ophthalmolgy Peshawar Medical College Peshawar."— Presentation transcript:

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3 Dr. Faizur Rahman Professor of Ophthalmolgy Peshawar Medical College Peshawar

4 At the end of the session the students would be able to:  Know various antibiotics and steroids used in Ophthalmic practice.  Describe the rationale of using various drugs.  Mechanism of action, effects and side effects of these drugs.  Know drug treatment of certain diseases

5  A chemical substance produced by one organism causing the death of other bacterial cells i.e penecillin and streptomycin.  After the introduction of synthetic agents these are now called antibacterials.  As newer agents came up now a wide spectrum of drugs are available called antimicrobials.

6  Difference between humans and microbes is exploited to produce substances toxic to microbes and harmless to humans.  The selective toxicity may be relative than absolute.  Concentration of antimicrobials must be carefully controlled.

7  INHIBIT BACTERIAL CELL WALL OR ACTIVATE ENZYMES THAT DESTROY BACTERIAL CELL WALL: ◦ PENICILLINS ◦ CEPHALOSPORINS ◦ BACITRACIN ◦ VANCOMYCIN ◦ KETOCONAZOLE ◦ MICONAZOLE

8  ALTER CELL WALL PERMEABILITY AND LEAKAGE OF INTRACELLULAR CONTENTS ◦ POLYMYXINS ◦ NYSTATIN ◦ AMPHOTERICIN B ◦ COLISTIMETHATE

9  INHIBIT PROTEIN SYNTHESIS ◦ Tetracyclines ◦ Aminoglycosides ◦ Macrolides/Ketolides ◦ Clindamycin ◦ Chloramphenicol

10  DRUGS THAT BLOCK SPECIFIC METABOLIC STEPS (Foleate inhibitors) ◦ SULFONAMIDES ◦ TRIMETHOPRIM  INHIBIT DNA DEPENDENT RNA POLYMERASE ◦ RIFAMPICIN

11  INHIBIT DNA DEPENDENT DNA SYNTHESIS ◦ QUINOLONES  ACT AS NUCLEIC ACID ANALOGUES ◦ ANTIVIRALS

12  Identify the infecting organism  Empiric therapy prior to identification  Determination of susceptibility  Barriers  Patient factors.  Safety of agent  Cost of therapy.

13  Chloramphenicol (Topical)  Anti-mycotics(Systemic and topical)  Aminoglycosides(Systemic and topical)  Sulphonamides(Systemic and topical)  Anti-virals (Systemic and topical)  Macrolides(Systemic)  Quinilones (Systemic and topical)  Cephalosporines (Systemic and topical)

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15 STEROIDS

16  Mineralo corticoids  Glucocorticoids  Androgens

17  Beciomethasone  Betamethasone  Cortisone  Des oxy cortico sterone  Dexamethasone  Fludro cortisone  Hydrocortisone  Methyl prednisolone  Para methasone  Prednisolone  Prednisone  Triamcinolone

18  Promote normal intermediary metabolism: Gluconeogenesis Stimulate protein catabolism Stimulate lipolysis  Increase resistance to stress by: Raising blood glucose level Modest rise in BP  Alter blood cell levels in plasma: Decrease in eosinophils, basophils, monocytes and lymphocytes by redistribution from circulation to lymphoid tissue Increase in the number of RBC, platelets, neutrophils

19  Anti inflammatory action: (Complex mechanism) Suppression of immunity Indirect inhibition of phospholipase A2  Alter other endocrine systems: Decrease in ACTH and TSH Increase in GH  Effects on other systems: Increased production of gastric acid, pepsin Effects on CNS Bone loss Myopathy

20  In the treatment of ocular inflammations and immune related ocular diseases.  Act by suppressing the formation of arachidonic acid and other mediators by induction mediators like phospholipaze A 2 and inhibitory protein Lipocorteins  Prevent edema, Fibrin deposition, capillary dilatation and proliferation, Leukocyte infiltration and subsequent scarring.

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22  Long acting/ Short acting/ Depot  Very potent  Potent  Moderately potent  Mild

23  Impaired wound healing/ Easy Bruising  Negative calcium balance/ Osteoporosis  Increased appetite/ Hyperglycemia/ Diabetes Mellitus  Euphoria/ Depression/ Psychosis  Hypertension  Edema (Sodium and water retension)/ Weight Gain  Peptic ulcers/ GI Hemorrhage/ GI Perforation  Hypokalaemia (Potassium depletion)  Hirsutism /Acne/ Coetaneous striae/ Amenorrhea  Myopathy (Gluconeogenesis)  Avascular Bone necrosis (Neck of femur)  Decreased Immunity

24  Cataract (PSC)  Steroid induced Glaucoma  Retinal Micro-Aneurysms  Papilloedema  Delayed Wound Healing  Mild Blephroptosis  Immune Suppression-Secondary Infections ◦ CANDIDA, TOXOPLASMOSIS, CMV, HSV,

25  Topical  Intralesional  Subconjunctival  Subtenon  Periocular  Intravitral  Intracameral  Systemic oral iv

26  Prenisolone (Topical and systemic)  Dexamethasone (Topical and systemic)  Betamethasone (Topical and systemic)  Hydrocortisone (Systemic only)  Loteprednol (Topical only) ( No IOP Rise)  Flouromethalone (Topical only) ( No IOP Rise)

27  Intra lesional in hemangioma and chalazion  Iv in optic neurirtis  Oral in dysthyroid ophthalmopathy. Corneal transplant  Intravitreal in CRVO  Topical postoperative, uveitis, corneal transplant  Intracameral Per-op in children

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33  The patient with orbital cellulitis should be promptly hospitalized for treatment. Hospitalization should be continued until the patient is afebrile and is clearly improved clinically.  Symptomatic; antipyretic, NSAIDS  Antimicrobials ; ◦ Ceftazidime 1 g tds, I/M ◦ Metronidazole 500mg tds, PO ◦ Vancomycin in case of allergy to the above mentioned  Surgical intervention in case of local abscess or unresponsive cases  Consultation with ENT specialist, neurosurgeon & paediatrician if required

34  Specifically identified pathogens identified on cultures.  Intravenous antibiotic therapy should be continued for 1-2 weeks and then followed by oral antibiotics for an additional 2-3 weeks.  Fungal infection requires intravenous antifungal therapy along with surgical debridement.

35 Surgical drainage of an orbital abscess is indicated if any of the following occurs:  A decrease in vision occurs.  An afferent pupillary defect develops.  Proptosis progresses despite appropriate antibiotic therapy.  The size of the abscess does not reduce on CT scan within hours after appropriate antibiotics have been administered.  If brain abscesses develop and do not respond to antibiotic therapy, craniotomy is indicated.

36 SAFE strategy developed by WHO for trachoma:  Surgery: ◦ To prevent blindness & limits progression of corneal scarring. ◦ Can improve vision.  Antibiotics: ◦ Azithromycin—1 G single dose (adults). ◦ Children: 20mg/kg single dose

37  Erythromycin 250 mg QID for 4 weeks. (children 125mg/kg).  Tetracycline 250 mg QID for 4 weeks.  Topical tetracycline 1% 0.5 inch ribbon BD for 6 weeks.  Facial cleanliness: ◦ Reduces risk & severity of trachoma.  Environmental change: ◦ Improved water supply & household sanitation. ◦ Personal & community hygiene. ◦ Adequate housing & water & sewage system.

38  Topical Tetracycline.  Oral Erythromycin 25mg/kg body weight 12 hourly for 14 days. Caution: Examine mother & father for chlamydial urethritis/ cervicitis and treat.

39  Broad spectrum antibiotics  Analgesics  Drainage if abscess formation

40  Initial treatment: Broad spectrum topical antibiotics (Fortified)  Dual therapy: Aminoglycoside & cephalosporin.  Mono therapy: Fluoroquinolone.  Oral antibiotics:  Atropine.  Systemic analgesics.

41 Acyclovir 3% ointment x 5 times daily Trifluorothymidine 1% drops 2-hourly Debridement if non-compliance or no response

42  Polyenes: Natamycin 5%: Filamentous fungi. Amphotericin B: Filamentous fungi.  Imidazole: Miconazole 1%: Candida, Aspergillus. Systemic: Itraconazole, Ketoconazole.  Pyramidine: Flucytosine 1%: Candida.

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44  Topical: Propamidine Isothionate 0.1% (Brolene), Dibromopropamidine Isothionate 0.15%, Miconazole 1%.  Systemic: Ketoconazole.

45 Intravitreal antiboitics Subconjuntival antibiotics. Topical antibiotics. Role of systemic antibiotics. Role of steroids. Role of vitrectomy. Cycloplegics and analgesics.

46 Drug Treatment of Glaucoma

47 To prevent further damage to the eye by lowering IOP & to ultimately prevent blindness

48  Plasma Expanders  Urea  Mannitol 20% IV solution. Dose: 1-2g/kg or 5 ml/kg body weight. Up-to 60 drops/min over min. Peak of action: within 30 min. Duration of action: up-to 6 hrs.  Diuretics  IV Acetazolimide

49  50% solution.  Oral agent with a sweet & sickly taste.  Pure lemon should be added to avoid nausea.  Dose:1-2g/kg or 2-4ml/kg body weight.  Peak of action: Within 1 hr.  Duration of action: Upto 3 hrs.  Metabolized to glucose in the body.

50  Oral agent with a minty taste.  Dose: Same as for glycerol.  Metabolically inert & can be given to diabetics without insulin cover.

51  Mechanism Of Action: 1- POAG: Stimulation of longitudinal muscle of ciliary body---pull on scleral spur---widening of trabecular spaces---lowering of IOP. 2- PACG: Opening the angle by pulling the peripheral iris away from the trabeculum.

52  Indications:  POAG.  Acute ACG.  Many secondary glaucomas. Good additive effect with beta blockers. Response: Blue eyes: Max. response. Dark eyes: Relatively low response.

53  Pilocarpine(1%,2%,3%,4%): One-half inch ribon at bed time. Induced myopia & miosis lasts only during sleep. Corneal haze in 20%, rarely affects VA.  Pilocarpine sustained-release (Ocusert Pilo-20 & Pilo-40): Polymer containing adsorbed pilocarpine. Inserted in upper fornix---7 days. Pilo-20: Equivalent to pilocarpine 1% drops. Pilo-40: Equivalent to pilcarpine 2-4% drops.

54  Parasympathomimetic muscarinic agonist, also a weak chloinesterase inhibitor. Onset of action: Within 40 min. Duration: 12 hrs. Dose: 8 hourly. Good alternative to pilocarpine in resistant cases. 0.01% intraocular solution for miosis during surgery.

55 Epinephrine Dipivefrin Clonidine Apraclonidine Brimonidine

56  Epinephrine 0.5, 1%, 2%  Mechanism Of Action: Increases both trabecular & uveoscleral outflow via beta agonist activity mediated by cyclic AMP.  Tripple response: Conj. decongestion, slight mydriasis & reduction of IOP.  Onset of action: Within 1 hr.  Duration of action: hr.  Indications: POAG, ocular hypertension.

57  Dipivefrin (0.1%)—(Propine)  Prodrug: Converted to adrenaline after absorption.  Penetration 17 times greater than adrenaline.  Duration of action same.  IOP lowering effect is comparable with 1% adrenaline.  Fewer side effects.

58  Twice daily dose.  Wash out period: 3.3 wks.  Peak effect at 2 hrs.  Duration of action 12 hrs.  Comparable to Timolol.  Nonresponder: Less than 10%.  No tachyphylaxis.  Good additivity to beta blockers, CAIs & miotics.  No vasoconstrictive effect in retinal tissues.

59  Prophylaxis of post-laser IOP spike.  Property of neuroprotection in animal models.  SIDE EFFECTS: Ocular: Follicular conj., contact dermatitis, ocular irritation & hyperemia. Systemic: Bradycardia, hypotension, apnea in neonates.

60  Pharmacokinetics:  Highly selective alpha-2 agonist.  Easy penetration to cornea.  Lower access to CNS: Less lipophilic, rapid metabolism, short plasma half life.  Reduce allergic reaction: Not produce hapten.  Mechanism Of Action: Reduce IOP by initial decreasing aqueous production followed by increase in uveoscleral flow.

61 OCULAR  Irritation.  Lacrimation.  Allergic BC.  Adrenochrome pigmentations.  Cystoid macular edema.  Pupillary dilatation. SYSTEMIC  Headache.  Palpitations.  Tachycardia.  Hypertensive crisis.  Anxiety.

62  Mechanism Of Action:  Decrease aqueous secretion with little effect on episcleral venous pressure.  10% unresponsive.  First choice medication for POAG.  Non-selective or cardioselective.  Contralateral effect.

63  0.25% and 0.50% BD.  Timolol LA 0.25% and 0.50%.  Digital pressure over eyes after medication (3minutes) to reduce systemic absorption.

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65  0.5% BD.  Cardio-selective.  Ocular hypotension < Timolol & Levobunolol & similar to Carteolol.  IOP reduction 6 mm Hg.  Less effective than Timolol in post-cataract surgery increase in IOP.  Increases retinal blood flow.  Superior visual fields protection.

66  Non selective.  Onset of action: Within 1 hr.  Peak of action: 2-6 hr.  Duration: 24 hr.  Dose: Usually OD.  Potent as Timolol.

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68  Non-selective.  More selective action on the eye than cardiopulmonary system. (less bradycardia than Timolol).  Efficacy similar to Timolol. Metipronolol (0.1%, 0.3%)  Non-selective.  Similar properties to Timolol.

69  Latonoprost (Latep)  Travoprost (Travatan)  Unoprostone (UF-021)  Bimatoprost (Lumigan)

70  Prodrug derived from pulmonary metabolite of PGF2 alpha.  Efficacy: 14-17% less than Latanoprost & comparable to Timolol.  Dose: 0.15% BD. Inhibit activity of endothelin-1 & may improve ocular blood flow.  Side effects: Conj. hyperemia, corneal epithelial defects.

71  Synthetic PGF2 alpha analog.  Dose: 0.004% OD.  Widest temperature storage range.  Efficacy: 7-8mm Hg IOP reduction (upto 33%)—start after 2 hr, peak at 12hr. 6-7mm Hg IOP reduction with Timolol. Higher mean IOP reduction & responder rate than Latanoprost.

72  Synthetic analog of endogenous prostamides.  Receptor profile: Controversial---no prodrug? no binding to PG receptors?  Mechanism Of Action: Increase trabecular outflow (35%) & uveoscleral outflow (50%).  Dose: 0.03% OD.  Efficacy: 33% (7-8mm Hg) IOP reduction. Better diurnal control & less PG-like side effects than Latanoprost.

73  Topical as well as systemic Acetazolamide 250mg Tablets (AZM) Brinzolamide Drops (Azopt) Dichlorphenamide 50 mg Methazolamide 50 mg

74  1) Timolol/ Dorzolamide (Cosopt) 2% dorzolamide & 0.5% timolol maleate. Efficacy: 25-30% IOP reduction (less than separate therapies).  2) Latanoprost/ Timolol (Xalacom) 0.005% latanoprost & 0.5% timolol,OD  3) Timolol/ Brimonidine (Combigan)  4) Timolol/ Pilocarpine.

75 THANK YOU


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