Definition
Risk factors
Physiology of aqueous secretion
Pathogenesis of glaucoma
Types of glaucoma
Treatment strategy
GLAUCOMA
Associated with raised intraocular pressure
( I.O.P > 21 mmHg)
Characterized by progressive optic nerve damage
and visual field loss
Risk factors
1. Raised IOP
2. Family H/o glaucoma
3. Myopia
4. Hypertension
Types of glaucoma
1. Open angle glaucoma
(wide angle, chronic simple)
2. Angle closure glaucoma
(narrow angle, acute congestive)
Treatment strategy
Lowers intra ocular tension by
1. decreasing aqueous humour secretion
2. increasing drainage of aqueous humour
Those which increases the
outflow of aqueous humour
• Cholinergic agoinsts – pilocarpine
• Cholinesterase inhibitor – physostigmine ,
demecarium , echothiophate
• Prostaglndin analogues – lantanoprost ,
unoprostone , travoprost , tafluprost
• Rho kinase inhibitor – netarsudi
Those which decrease the production of aqueous humor by
the ciliary body
• Non selective beta adrenergic blockers – timolol
• Selective beta 1 – adrenergic blocking agents –
betaxolol , careteolol , levobunolol
• Non selective adrenergic agonists – adrenaline
hydrochloride
• Selective alpha 2 adrenergic agonists – apraclonidine ,
brimonidine
• Carbonic anhydrase inhibitor – topical – brinzolamide
systemic – acetazolamide
• Combination – brinzolamide +brimonidine , timolol
+brimonidine ,timolol + dorzolamide
Open angle glaucoma
 Genetically predisposed
 Degenerative
 Affects patency of trabecular meshwork
Ocular hypotensive drugs to be used
1. β blockers
2. miotics
3. α adrenergic agonists
4. carbonic anhydrase inhibitors
Topical β blockers
First choice drug
Lower IOP by reducing aqueous formation
Inhibit cAMP pathway in the ciliary process
Highly lipophilic
Non-selective
Timolol
Levobunolol
Metipranolol
cartiolol
Selective
Betaxolol
Advantages
 No change in pupil size
 No induced myopia
 No headache/brow pain
 No fluctuation in IOP
 Convenient
Prostaglandins
1st line drug
PGF2α derivative
Latanoprost, Isopropyl unoprostone
Increases uveoscleral outflow
Advantages over β blockers
 Once daily dosing
 Low systemic side effects
 Potent IOP lowering effect
α adrenergic agonists
Clonidine congeners
Brimonidine - more α2 selective, highly lipophilic
Apraclonidine - highly ionised
 Reduces aqueous secretion &
 Increases uveo – scleral outflow
 Ocular side effects are less
 Indicated for short & long term use in glaucoma
Miotics
Increase
 tone of ciliary muscle & sphincter pupillae
 trabecular outflow
Pilocarpine (0.5%)
Preferred miotic
Action is rapid & short acting (4 – 6 h)
Disadvantages
Diminution of vision, spasm of accommodation, brow pain,
nausea, diarrhoea, sweating, bronchospasm
Ocusert – long acting, once daily
Physostigmine (0.1%) - supplement to pilocarpine
Potent & long acting miotics (demecarium,
echothiophate) - accelerate cataract development
Used only as add on therapy
Effective in aphakic glaucoma
Carbonic anhydrase inhibitors
Acetazolamide
Reduces aqueous formation by limiting
generation of bicarbonate ion in the ciliary
epithelium
Used to supplement ß blockers and other ocular
hypotensive drugs
Systemic side effects: paresthesia, anorexia,
hypokalemia, acidosis
Dorzolamide, Brinzolamide
Combination treatment
 Improves compliance
 Reduces number of drops to be instilled
If Combination treatment fails
oral acetazolamide is given followed by surgery
Angle closure glaucoma
 Narrow iridocorneal angle
 Shallow anterior chamber
 Emergency condition
1. Topical β blocker: Timolol 0.5% instilled 6-8th hrly
2. Miotic: pilocarpine 1-2% instilled every 10 min;then at long
intervals
3. Hypertonic mannitol (20%) or glycerol (10%)
4. Acetazolamide 0.5g iv or oral twice daily
5. Apraclonidine 1% / latanoprost 0.005% / brimonidine 0.2%
Alzheimer’s disease
First characterized by Dr. Alois Alzheimer (1907)
Neurodegenerative disorder characterized by progressive
dementia primarily affecting cholinergic neurons in the brain
 Affects cognition & behaviour
 Etiology unknown
 No cure exists
 Pharmacotherapy aims at reducing symptoms
Risk factors
Age
Prevalence increases with age
 65 – 75 yrs: 7%
 75 – 84 yrs: 53 %
 >85 yrs
: 40%
Sex
More common in women
Others
Head injury, stroke, alcohol, illiterate
Cerebroselective Anti-ChE
Tacrine
: hepatotoxic
Rivastigmine : 6 -12 mg/day
Donepezil
: 5- 10 mg/day
Galantamine : 24 mg/day
Primary intervention: Non pharmacological & social support
Treatment of cognitive symptoms
Cholinesterase inhibitors – to be given throughout
NMDA receptor antagonist - Memantine
Symptomatic approach to psychiatric problems
Others
 Vitamin E
 Selegiline
 Estrogen
 Anti-inflammatory
Nicotine
• Tobacco plant
• MOA – agoinst at cholinergic receptor in
brain ,autonomic ganglia and NMJ
• Nm – skeletal neuromuscular junction
• Nn – CNS and autonomic ganglia
• Release – ACh ,NA, DA, 5HT , and beta
endorphin in CNS
• GH, prolactin and ACTH
PHARAMACOLOGICAL
ACTIONS
• Behavioral effects – stimulation in low
dose mesolimbic system
• Attention ,learning , reaction time problem
solving
• Smokers – pleasure relaxation and
reduction in anger tension depression and
stress
• CNS – tremors ,convulsions large dose –
depression
• CTZ – Vomiting
• CVS – increses heart rate due to
increased release of catecholamines
following stimulation of the sympathetic
ganglia and adrenal medulla
• GIT – nicotine increases the motility tone
and secretion of the GIT TRACT colonic
evacuation stimulation of parasympathetic
ganglia
• Salivation and bronchial secretion
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•
•
•
•
•
Carcinoma of lungs
Chronic bronchitis and emphysema
COPD
IHD
PVD
GIT disturbances
Tobacco dependence
• Nicotine receptor agonists – transdermal
patches , polacrylate gum/lozenges ,
nicotine nasal spary ,oral inhaler
• Partial agoinst – vareniciline
• Doapmine / NA central reuptake inhibitor –
bupropion