Optho Pharm (Imported from Leah) Flashcards
Sympathetic Nervous System: -cell body origin -Effect: generalized or localized
generalize massive effect originating T1-L2
Parasympathetic Nervous System: -cell body origin-Effect: generalized or localized
CN3,7,9,10// S2-4 output more localized/ specific effects
Where are nicotonic receptors located?
-parasympathetic and sympathetic ganglionic synapses (Nn) -NMJ/ skeletal muscle: (Nm)
Where are muscarinic receptors located?
-parasympathetic end organs (Ach)-sympathetic input to sweat glands
Iris sphincter vs dilator: (shape)
sphincter- circular muscle dilator- radial
Describe the process of accomodation:
-near stimulus -contracture of ciliary muscle -loosening of the zonules -thickening of lens
Define: cycloplegia
paralysis of ciliary muscle= inability to accomodate
stimuli spasm of accomodation: overstimulation of ciliary muscle/ chronic accomodation= blurring, pain
Function of the aqeuous humor
-nutrients -mechanical stability/ provides healthy IOP
Normal tension glaucoma:
glaucoma in the presence of normal intraocular pressure
“Normal” IOP: **I think Egleton wont be testing us on this, so I wont be memorizing specific DISEASE values. In real life + according to Fry, levels vary person to person.
8-20 mmHg
1-3rd order sympathetic innervation of the eye:
1: hypothalamus –> ciliospinal center of budge (C8-T2)
2: sympathetic chain –> superior cervical ganglion
3: axons ride cartoids to targets
What sympathetic axons travel along ECA? ICA?
ECA: sweat glands of face below forehead
ICA: others (muller, dilator, sweat glands forehead)
Parasympathetic innervation of the eye?
E.W. nucleus –> interpeduncular fossa midbrain /CN3 (medial fibers)
CN3 (inferior dvsn) –> ciliary ganglia –>branches travel with CN2 (short posterior ciliary nerves)–> target (sphincter/ ciliary muscle)
Iris dilator: main receptor:
a1
muellers muscle: main receptor:
a1
ciliary process: main receptor:
mainly B2 *some B1, a2
conjunctival blood vessels: main receptor:
a1
ciliary muscle/ iris sphincter: main receptor
muscarinic
Lacrimal gland: main receptor
a1
Rank relative % of all ophthalmic meds administered via each ROAs (6)
topical > intravitreal / retrobulbar > subtenton > oral > IV
Phenylephrine:
MOA
Use (3 ophtho use, 1 general use) general side effects?
3 ophtho ADRS
a1 agonist
- induces mydriasis for fundoscopic exam
- vasoconstriction (2.5%) = can differentiate scleritis from episcleritis
- separate iris from lens when stuck together (synechia, seen in uveitis) (10%)
- nasal decongestion Optho
ADRs:-a1 systemic effects + lid retraction, lacrimation, angle closure in eye
Epinephrine historical use in ophtho:
primary therapeutic of disease (glaucoma) until timolol B blocker was released *reason/ mechanism has many theories, only mildly effective, NOT used any longer *MANY sympathetic ADRs
Why isn’t epinephrine effective for mydriasis/ fundoscopic exam?
melanin of iris binds epi (inhibits its action on pupillary muscles)
*results in Iris/Lens pigmentation from Epi deposits
Most dangerous effects of epinephrine on the eye? (3)
- increased IOP-angle closure= EMERGENCY
- cystoid macular edema: decreased acuity/ possibly
- PERMANENT VISION LOSS
Even in the presence of phenylephrine, accomodation + light reflex can still occur. Why? How is this blocked for surgeries/ exams?
-parasympathetic system still intact! * ciliary muscle and iris sphincter have largely muscarinic receptors (few a1, so phenylephrine does not block) * must co-administer anticholinergic
Apracyclonidine:
- MOA & drug it is derived froM
- Most common ophtho use
- ocular side effects
-a agonist, some a2 selectivity clonidine derivative
-used to rapidly reduce IOP
-same side effects as phenylephrine due to slight a1 agonistic properties
++ ALLERGIC POTENTIAL
3 ways that apracyclodine may treat increased IOP:
1) reduces presynaptic NE release at ciliary process
2) reduced intracellular cAMP in ciliary process epi cells 1-2 = decreased AH production
3) a2 receptors on episcleral vein = ^^ AH outflow
Why isnt apracyclodine used to chronically treat glaucoma?
significant drift/ loss of efficacy over time; only use to emergently decrease IOP
Brimonidine MOA **First line treatment for: -2nd line treatment for: -Allergic potential -Side effects
- highly (most) selective a2 agonist
- *1st line NTG treatment
- 2nd line for open angle glaucoma
- low allergic potential
- side effects are parasympathetic (dry mouth, HA, lethargy)
Open angle glaucoma first line treatments: (2 general categories)
B blockers and prostaglandins
How is brimonidine “neuroprotective” to the optic nerve?
a2 stimulation- vasodilation- increased blood supply to CN2
**What condition is cocaine used to diagnose? How?What concentration is used?
Blocks NE reuptake; should induce myrdriasis, can be used to diagnose Horner’s Normal response in eye –> (dilation) healthy No dilation –> Possible Horner’s patient *4-10%
Hydroxyamphetamine MOA + What condition is it used to diagnose? How?
- Causes NE release from post-ganglionic neurons–> iris dilator *Differentiates pre vs post ganglionic Horner’s syndrome
- Pre: pupil responds (dilates) = SERIOUS
- Post: no response= less serious
Causes of pre-ganglionic Horner’s? (3)
1- tumor at apex of lung (Pancoasts)
2- thoracic aortic aneurysm
3- carotid endarterectomy
Causes of post- ganglionic Horner’s (2)
1-goiter
2-cavernous sinus syndrome
Dapiprazole: MOAUse ADR (2)Still Used?
MOA: a-block
Tx: reverses clinically (phenylephrine) induced dilation
ADR: hyperemia of conjunctival vessels, ptosis
*no longer used because short shelf life and $$$
Timolol MOA **Use (Gold Standard For?) Dosing? Benefits? (3) Don't give it to who?
- B blocker (1+2)- blocks B2»> at ciliary muscle to decrease production of AH–> Decrease IOP
- Gold standard for OPEN ANGLE GLAUCOMA
- once daily dosing
- minimal drift, no dilation, good additive effect with other meds
- NOT FOR ASTHMATICS**
What are levobunolol and metipranolol?
Derivatives of timolol
-levobutol has longer duration of action than timolol
Contraindications to use of timolol, levobunol, or metipranolol? Optho related ADRs?
- COPD/ asthma/bronchitis (B2 block)
- CHF
-ADR: minimal, some corneal anesthesia
Betaxolol:
MOA
Use
- selective B1 block
- treats glaucoma safely in patients with COPD/ Asthma (“Bettah 1, makes breathing less TAXing”)
- Still contraindicated in CHF
Cartelol:
MOA
Use
**Special because?
Competes with NE/Epi at B receptors technically “sympathomimetic” but only 1-2% as effective as NE/Epi so works as NON SPECIFIC B-BLOCK
**Only B blocker that has intrinsic sympathetic activity
Rank ophtho B blocks in terms of potency
cartelol >timolol/levobunolol>betaxol > metipranolol
Use for all B blockers in ophtho?
glaucoma treatment decreases AH output from ciliary processes by blocking B receptors (B2»>)
(Decrease Adenylate Cyclase/ cAMP pathway activity)
Three drugs that may induce miosis/ reduce IOP?
What is their class/action?
What is their ROA?
cholinergic agonists
pilocarpine- topical
acetylcholine/ carbachol- injections
**Pilocarpine important use?
Two special characteristics (Duration of action? metabolism?)
- Breaks ANGLE CLOSURE in glaucoma acute attack (mechanically pulls iris out of way to enable drainage into TM–>schlemm canal)
- some use in open angle
- long lasting, not broken down by AchE
Pilocarpine-ADRs (general trend + 2 important systemic): ADRs 2 ophtho:
Systemic: SLUDE BBB + pulmonary edema and mental status change
Optho: accommodation spasm (under 40yrs) + miosis (dimming of vision/ restricted peripheral vision)
When is acetylcholine used and why is it rare?
intraocular injection for some surgeries
quickly metabolized by AchE so miosis effects are very short lasting
When is carbachol used?
important consideration?
complicated cataract surgery to keep lens in posterior chamber (effects last up to 24hrs)
(“Carbachol buckles the lens down”)
*same side effects as pilocarpine but more SEVERE SLUDE BBB
Physostigmine and neostigmine:
MOA
When are they used ?
AchEi
short acting used to rescue from acute angle closure glaucoma if patient is ALLERGIC to pilocarpine (rare)
Echothiopate and Isofluorophate:
MOA
Why not used ?
Organic AchEi (phosphorylates the enzyme)=IRREVERSIBLE ***severe ADRs (^^^SLUDE BBB + retinal detachment, cataracts, iris cysts etc)
Four uses for cholinergic antagonists?
- mydriasis
- cycloplegia (ciliary muscle inhibition- gets rid of accomodation for surgery)
- Accommodative Esotropia (infants + kiddos)
- uveitis/ inflammation- relieve pain, decrease risk posterior synechia to lens
Tropicamide: MOA Use (combined with?) Not good for? Safe for?
anti-cholinergic
- mydriasis/Retinal Exam
- combined with phenylephrine
- Not good for cycloplegia- inhibits light, but not accommodation response
- Safe for Glaucoma Pt
cyclopentolate:
MOA
Use for
anticholingeric mydriasis + cycloplegia
*SURGERY because long lasting + loss of accomodation (not comfortable for patient during standard exam)
Homatropine:
MOA
Use
anti-cholinergic
mydriasis + cycloplegia
PAIN RELIEF (uveitis)
effects last even longer than cyclopentolate
*reduces amount of inflammatory modulators
mechanically forced from vessels during contraction
Atropine
MOA
Use in ophtho (2)
*****Avoid in what two populations?
anti-cholinergic EXTREME cycloplegia and mydriasis
- Exam for infants/ children
- Treats accommodative esotropia in children
*****Down syndrome or Glaucoma
What is accommodative esotropia?
Why is atropine effective treatment?
Disease causes eye to turn inward because of excess accommodation (stimulating convergence)
*Atropine causes cycloplegia (prevents accomodation)
Which anti-cholinergic is most contraindicated in glaucoma?
Which is safe for glaucoma?
atropine= serious effects
tropicamide has low efficacy and is safe in glaucoma
Rate length of mydriasis/cycloplegia for each of the four anti-cholinergics?
atropine > homatropine > cyclopentolate > tropicamide atropine = 288 hours- 12 DAYS
Rate amount of mydriasis achieved for each of the four anti-cholinergics?
atropine > tropicamide> cyclopentolate > homatropine
Which anti-cholinergic requires the highest concentration for effect?
homatropine(5%) - all others need 1%
How to diagnose parasympathetic damage to eye? (Blown pupil)
use pilocarpine (as long as there is no trauma)
- see dilation= Addie’s Tonic Pupil
- no dilation= could be pharmacologic
- see miosis= tumor, aneurysm etc
How long does it take for tropicamine to reach max mydriasis?
how long does mydriasis last?
20-30 min
4 hours
