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Glaucoma
 It is a heterogenous group of diseases in which
damage optic nerve (optic neuropathy).

 is usually caused by raised ocular pressure (normal
IOP is 15.5 mmHg) acting on the nerve head.

 characterized by:

 optic nerve damage       cupping of the optic disc
  and subsequent loss of retinal nerve fibre.
EPIDEMIOLOGY :
 In the world, glaucoma is the third
leading cause of blindness.

 an estimated 13.5 million people may
have glaucoma and 5.2 million of those
may be blind.
Classification of glaucoma
Primary glaucoma:
   Open angle glaucoma
   Closed (narrow) angle glaucoma

Secondary glaucoma :
  •Traumatic glaucoma
  •Pigmentory depression glaucoma
  • glaucoma associated with other ocular diseases (uveitis)
  •Raised episcleral venous pressure
  •Steroid induced glaucoma
  •Neovascular glaucoma
  •Psedoexfoliation glaucoma

  •Congenital glaucoma
open angle glaucoma


  it also called chronic simple or wide angle glaucoma

  It is the most common type of glaucoma.


 • It affects approximately 1 in 200 of
 population over the age of 40 years.
cause and mechanism of open angle:

   it occurs as a complication of chronic obstruction in
   the trabeculare meshwork.
   -It causes slow damage to the optic nerve.

             Symptoms:
   - most time is symptomless
    characterized by:
     -Cupped optic disc
    -Gradual loss of peripheral vision
    -Tunnel vision in the advanced stage
Close angle glaucoma

  -also called acute or narrow angle glaucoma.
  -occurs in small eyes (as in hyperopoia) with
  shallow anterior chambers.

       Cause and mechanism :
   iris dilation      the lens sticks to the back of the iris
      prevent fluid flow from posterior to anterior
   chambers

   Fluid accumulati0n         preventing drainage

    rapid     IOP
Symptoms :
1-eye redness and painful.
2-Blurred vision.
3-Patient may notice haloes (circles of light) around
light.
Secondary glaucoma :

   Pigmentory depression glaucoma:

   Pseudoexfoliative glaucoma:

   neovascular glaucoma:

   Steroid induced glaucoma:

   trauma

     uveitis
Congenital glaucoma
 It present at birth.
 due to the abnormal development of the anterior
  chamber angle before birth.
 this causes decrease in aqueous outflow    IOP
          loss of vision..


               Symptoms

    Tearing                   Bupthalmus
    Light sensitivity        Cloudy cornea
Risk factors for glaucoma

*Age                       *Diabetes


*Family history            *Thin cornea


*Previous eye injury       *Vasospasm


*Systemic HTN              *myopia
Risk factors for glaucoma

*Age                   * Family history

*Previous eye injury   *myopia    *


*Diabetes              *Thin cornea

*Systemic HTN          *Vasospasm
The goal of glaucoma treatment
  preserve the visual field .

  prevent the loss of visual function .


 achieved by :
 Medication
 Laser therapy

 Conventional surgery
Strategies of treatment

 1-Decreasing Production of Aqueous
 Humor.

 2-Increasing Outflow of Aqueous
 Humor.
pharmacologicaal treatment:

   we have 5 classes of drugs :

   1- Beta blockers

2-alpha agonist (alpha-2 agonist and non specific agonist)

 3-carbonic anhydrase inhibitors

  4- Parasympathomimetics.

   5- prostaglandin analogs
Also it can be classified as:
1-drugs that decrease aqueous humor production:
      Beta blockers.
      alpha2 –agonists.
      carbonic anhydrase inhibitors

2- drugs that increase aqueous humor outflow:
       prostaglandin analoges

      non specific adrenergic agonists
      cholenergics (Parasympathomimetics)
Site of action of anti glaucoma drugs :




1-miotic 2-=miotic 3-Beta blocker 4-prostaglandine adrenaline 5-adrenaline
Drug used for open angle
beta blockers
alpha agonists


drug used for close angle
1- Beta blockers:

first choice for initial and maintenance treatment of open-angle.

 for ocular HTN.


 They block Beta receptor in iris and ciliary body
  aqueous humor production              IOP.


Classify in to:


 elective B1-blockers       . Betaxolol, atenolol and metoprolol


non-selective B-blockers timolol , nadolol, befunolol, carteolol,
                          penbutolol, labetalol, nipradilol.
Side effects:
low BP.                     cardiac arrhythmias
cardiac insufficency        reduced pulse rate



            Contraindications

Cardiogenic shock
Over cardiac failure
 Sinus bradycardia
 history of COPD
 Second and third degree AV block
2-alpha agonists
A_ Alpha-2 Adrenergic Agonists :(apraclonidine, brimonidine)
 MOA
          IOP by reducing production of aqueous humour.
Side effects:
HTN
tachycardia
allergic conjunctivitis
local irritation
head ache

  dose:
         Apraclonidine : 1-2 drops tid.

         brimonidine: : 1 drop every 8 hr.
contraindications of Alpha-2 Adrenergic


•Breast-feeding
• Closed-angle glaucoma
• Heart disease
• Liver disease
•Eye infection or damage
•Kidney disease
•Pregnant or trying to get pregnant
B_non specific adrenergic agonists
    (epinephrine, dipivefrin)

Epinephrine
 MOA:

     aqueous humor formation

     trabecular outflow. (stimulate alpha-2)


 Onset : 1 hr
 dose:   twice daily.

 side effects : -HTN
           -                          - allergic lid reactions
                - browache,            -conjunctival hyperemia
Dipivefrine

  • is the prodrug of epinephrine.
  • better tolerated than epinephrine.

side effects:   follicular conjunctivitis.



Contraindications of epinephrine and dipivrfrine

 • not be used in patients with narrow angles since any
 dilation of the pupil may predispose the patient to an attack
 of angle-closure glaucoma
3-carbonic anhydrase inhibitors:
  (acetazolamide, methazolamide, dichlorphenamide,
  brinzolamide , dorzolamide )

  MOA
 reduce HCO3 &H2O content of aqeous humor
 by secretion of them from the eye.

           Administration:
   o Orally (Rx. open angle glaucoma )
   o IV or IM ( preoperatively for closed angle glaucoma
     (acetazolamide))
   o Topically
Side Effects
  -aplastic anemia
 -allergic reaction
 -electrolyte disorder
 -renal or hepatic insuffecency

  Contraindications/Precautions:
   ◊ hepatic disease (may precipitate hepatic coma)
   ◊ renal or adrenocortical insufficiency
   ◊ hyponatremia
   ◊ hypokalemia
   ◊ hyperchloremic acidosis or electrolyte imbalance.
4-Parasympathomimetics
  [pilocarpine, carbachol, echothiophate]
  →In the past, miotics were DOC
   but currently due to their high side-effects, their use has
  declined.
                   Mechanism:
   pupil size         drainage of intraocular fluid -increasing
   the flow of intraocular fluid from the eye…
                       or
 by contraction of ciliary body muscle             Increases
 drainage of intraocular fluid.
                 Administration:
                 Topical drops and gel.
Pilocarpine :
→is the principal alkaloid .
the miotic action of the drug relieves the pupillary block
and also pulls the iris away from the anterior chamber angle
→ It increases the trabecular outflow due to cilliary body contraction.
Its onset of action is rapid, peak effect occurs between 30-60
minutes and lasts for 4-8 hours


Side Effects of this class

* Headache                 * induced miopia.
* Many people complain of dim vision, especially at night or in
darkened areas such as movie theaters. This is due to constriction
of the pupil.

 Dose: 1-2 drops up to 6 time/ day to control intraocular pressure
5- prostaglandin analogs:
 (latanoprost, bimatoprost, unoprostone, travoprost)

 MOA :
 increase the uveoscleral outflow.
  Side Effects:
  -Iris pigmentation
  - local irritation
  -increased growth of eyelashes
               Latanoprost:
   →Its maximum effet is achieved at 12 hrs
   →the best time for using it is at 9 pm,because the maximum
   IOP lowering effect is after 12 hrs. i.e. at 9 am(and thats also
   the time when IOP is at its peak)
Unoprostone :

› it is the first docosanoid derivative for glaucoma therapy.
› It acts by enhancing uveoscleral outflow without
affecting aqueous humour production

 › It is available as 0.12% ophthalmic solution
Dose: requires twice a day instillation

side effects of this class :
                         •iritits
                         • ncrease iris pigmentation
                         •conjunctival pigmentation
                         •cytosoid macular edema
Combination:
Combigan®
       is a combination of beta blocker and alpha agonist
      (Brimonidine &Timolol )


Cosopt®
    is a combination of beta blocker and carbonic anhydrase
   inhibitor(dorzolomide & timolol ).
 Mechanism; Decreases production of intraocular fluid

 Side Effects:

Side effects of Combigan® include the symptoms of beta blockers and
alpha agonists
Side effects of Cosopt® include burning and/or stinging of the eyes and changes in
sense of taste.
Category        MOA           Drugs                 Side effect
Β-adrenergic    Decrease      Timolol               systemic effect (bronchospasm,
blockers        aqueous       Levobunolol           bradycardia, heart block,
                formation     Metrapranolol         hypotension..)


Cholinergic     Increase      Pilocarpine           Miosis, decrease night vision,
stimulation     aqueous       Carbachol             headache, increase GI motility,
                outflow                             decreased heart rate

Adrenergic      Both          Epinephrine HCl       Contact allergy, hypotension in
stimulating                   Dipivitrin            children
                              Brimonidine

Carbonic        Decrease      Oral acetazolamide    Renal calculi, nausea, vomiting,
anhydrase       aqueous       Topical dorzolamide   diarrhea, weight loss, aplastic
inhibitor       formation                           anemia, BM suppression
                                                    S/E generally absent with topical
                                                    preparation

Prostaglandin   Improve       Latanoprost           Iris color change, lash growth,
agonists        uveoscleral                         trichiasis
                outflow
The end slide
Thank you

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Glaucoma

  • 1.
  • 2. Glaucoma  It is a heterogenous group of diseases in which damage optic nerve (optic neuropathy).  is usually caused by raised ocular pressure (normal IOP is 15.5 mmHg) acting on the nerve head.  characterized by:  optic nerve damage cupping of the optic disc and subsequent loss of retinal nerve fibre.
  • 3. EPIDEMIOLOGY :  In the world, glaucoma is the third leading cause of blindness.  an estimated 13.5 million people may have glaucoma and 5.2 million of those may be blind.
  • 4. Classification of glaucoma Primary glaucoma: Open angle glaucoma Closed (narrow) angle glaucoma Secondary glaucoma : •Traumatic glaucoma •Pigmentory depression glaucoma • glaucoma associated with other ocular diseases (uveitis) •Raised episcleral venous pressure •Steroid induced glaucoma •Neovascular glaucoma •Psedoexfoliation glaucoma •Congenital glaucoma
  • 5. open angle glaucoma it also called chronic simple or wide angle glaucoma It is the most common type of glaucoma. • It affects approximately 1 in 200 of population over the age of 40 years.
  • 6. cause and mechanism of open angle: it occurs as a complication of chronic obstruction in the trabeculare meshwork. -It causes slow damage to the optic nerve. Symptoms: - most time is symptomless characterized by: -Cupped optic disc -Gradual loss of peripheral vision -Tunnel vision in the advanced stage
  • 7. Close angle glaucoma -also called acute or narrow angle glaucoma. -occurs in small eyes (as in hyperopoia) with shallow anterior chambers. Cause and mechanism : iris dilation the lens sticks to the back of the iris prevent fluid flow from posterior to anterior chambers Fluid accumulati0n preventing drainage rapid IOP
  • 8. Symptoms : 1-eye redness and painful. 2-Blurred vision. 3-Patient may notice haloes (circles of light) around light.
  • 9. Secondary glaucoma :  Pigmentory depression glaucoma:  Pseudoexfoliative glaucoma:  neovascular glaucoma:  Steroid induced glaucoma:  trauma  uveitis
  • 10. Congenital glaucoma  It present at birth.  due to the abnormal development of the anterior chamber angle before birth.  this causes decrease in aqueous outflow IOP loss of vision.. Symptoms  Tearing  Bupthalmus  Light sensitivity  Cloudy cornea
  • 11. Risk factors for glaucoma *Age *Diabetes *Family history *Thin cornea *Previous eye injury *Vasospasm *Systemic HTN *myopia
  • 12. Risk factors for glaucoma *Age * Family history *Previous eye injury *myopia * *Diabetes *Thin cornea *Systemic HTN *Vasospasm
  • 13. The goal of glaucoma treatment  preserve the visual field .  prevent the loss of visual function . achieved by : Medication Laser therapy Conventional surgery
  • 14. Strategies of treatment 1-Decreasing Production of Aqueous Humor. 2-Increasing Outflow of Aqueous Humor.
  • 15. pharmacologicaal treatment: we have 5 classes of drugs : 1- Beta blockers 2-alpha agonist (alpha-2 agonist and non specific agonist) 3-carbonic anhydrase inhibitors 4- Parasympathomimetics. 5- prostaglandin analogs
  • 16. Also it can be classified as: 1-drugs that decrease aqueous humor production: Beta blockers. alpha2 –agonists. carbonic anhydrase inhibitors 2- drugs that increase aqueous humor outflow: prostaglandin analoges non specific adrenergic agonists cholenergics (Parasympathomimetics)
  • 17. Site of action of anti glaucoma drugs : 1-miotic 2-=miotic 3-Beta blocker 4-prostaglandine adrenaline 5-adrenaline
  • 18. Drug used for open angle beta blockers alpha agonists drug used for close angle
  • 19. 1- Beta blockers: first choice for initial and maintenance treatment of open-angle. for ocular HTN. They block Beta receptor in iris and ciliary body aqueous humor production IOP. Classify in to:  elective B1-blockers . Betaxolol, atenolol and metoprolol non-selective B-blockers timolol , nadolol, befunolol, carteolol, penbutolol, labetalol, nipradilol.
  • 20. Side effects: low BP. cardiac arrhythmias cardiac insufficency reduced pulse rate Contraindications Cardiogenic shock Over cardiac failure Sinus bradycardia history of COPD Second and third degree AV block
  • 21. 2-alpha agonists A_ Alpha-2 Adrenergic Agonists :(apraclonidine, brimonidine) MOA IOP by reducing production of aqueous humour. Side effects: HTN tachycardia allergic conjunctivitis local irritation head ache dose: Apraclonidine : 1-2 drops tid. brimonidine: : 1 drop every 8 hr.
  • 22. contraindications of Alpha-2 Adrenergic •Breast-feeding • Closed-angle glaucoma • Heart disease • Liver disease •Eye infection or damage •Kidney disease •Pregnant or trying to get pregnant
  • 23. B_non specific adrenergic agonists (epinephrine, dipivefrin) Epinephrine MOA: aqueous humor formation trabecular outflow. (stimulate alpha-2) Onset : 1 hr dose: twice daily. side effects : -HTN - - allergic lid reactions - browache, -conjunctival hyperemia
  • 24. Dipivefrine • is the prodrug of epinephrine. • better tolerated than epinephrine. side effects: follicular conjunctivitis. Contraindications of epinephrine and dipivrfrine • not be used in patients with narrow angles since any dilation of the pupil may predispose the patient to an attack of angle-closure glaucoma
  • 25. 3-carbonic anhydrase inhibitors: (acetazolamide, methazolamide, dichlorphenamide, brinzolamide , dorzolamide ) MOA reduce HCO3 &H2O content of aqeous humor by secretion of them from the eye. Administration: o Orally (Rx. open angle glaucoma ) o IV or IM ( preoperatively for closed angle glaucoma (acetazolamide)) o Topically
  • 26. Side Effects -aplastic anemia -allergic reaction -electrolyte disorder -renal or hepatic insuffecency Contraindications/Precautions: ◊ hepatic disease (may precipitate hepatic coma) ◊ renal or adrenocortical insufficiency ◊ hyponatremia ◊ hypokalemia ◊ hyperchloremic acidosis or electrolyte imbalance.
  • 27. 4-Parasympathomimetics [pilocarpine, carbachol, echothiophate] →In the past, miotics were DOC but currently due to their high side-effects, their use has declined. Mechanism: pupil size drainage of intraocular fluid -increasing the flow of intraocular fluid from the eye… or by contraction of ciliary body muscle Increases drainage of intraocular fluid. Administration: Topical drops and gel.
  • 28. Pilocarpine : →is the principal alkaloid . the miotic action of the drug relieves the pupillary block and also pulls the iris away from the anterior chamber angle → It increases the trabecular outflow due to cilliary body contraction. Its onset of action is rapid, peak effect occurs between 30-60 minutes and lasts for 4-8 hours Side Effects of this class * Headache * induced miopia. * Many people complain of dim vision, especially at night or in darkened areas such as movie theaters. This is due to constriction of the pupil. Dose: 1-2 drops up to 6 time/ day to control intraocular pressure
  • 29. 5- prostaglandin analogs: (latanoprost, bimatoprost, unoprostone, travoprost) MOA : increase the uveoscleral outflow. Side Effects: -Iris pigmentation - local irritation -increased growth of eyelashes Latanoprost: →Its maximum effet is achieved at 12 hrs →the best time for using it is at 9 pm,because the maximum IOP lowering effect is after 12 hrs. i.e. at 9 am(and thats also the time when IOP is at its peak)
  • 30. Unoprostone : › it is the first docosanoid derivative for glaucoma therapy. › It acts by enhancing uveoscleral outflow without affecting aqueous humour production › It is available as 0.12% ophthalmic solution Dose: requires twice a day instillation side effects of this class : •iritits • ncrease iris pigmentation •conjunctival pigmentation •cytosoid macular edema
  • 31. Combination: Combigan® is a combination of beta blocker and alpha agonist (Brimonidine &Timolol ) Cosopt® is a combination of beta blocker and carbonic anhydrase inhibitor(dorzolomide & timolol ). Mechanism; Decreases production of intraocular fluid Side Effects: Side effects of Combigan® include the symptoms of beta blockers and alpha agonists Side effects of Cosopt® include burning and/or stinging of the eyes and changes in sense of taste.
  • 32. Category MOA Drugs Side effect Β-adrenergic Decrease Timolol systemic effect (bronchospasm, blockers aqueous Levobunolol bradycardia, heart block, formation Metrapranolol hypotension..) Cholinergic Increase Pilocarpine Miosis, decrease night vision, stimulation aqueous Carbachol headache, increase GI motility, outflow decreased heart rate Adrenergic Both Epinephrine HCl Contact allergy, hypotension in stimulating Dipivitrin children Brimonidine Carbonic Decrease Oral acetazolamide Renal calculi, nausea, vomiting, anhydrase aqueous Topical dorzolamide diarrhea, weight loss, aplastic inhibitor formation anemia, BM suppression S/E generally absent with topical preparation Prostaglandin Improve Latanoprost Iris color change, lash growth, agonists uveoscleral trichiasis outflow