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Neuro-Psych Exam II > Optho Pharm (Imported from Leah) > Flashcards

Optho Pharm (Imported from Leah) Flashcards

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1
Q

Sympathetic Nervous System: -cell body origin -Effect: generalized or localized

A

generalize massive effect originating T1-L2

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2
Q

Parasympathetic Nervous System: -cell body origin-Effect: generalized or localized

A

CN3,7,9,10// S2-4 output more localized/ specific effects

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3
Q

Where are nicotonic receptors located?

A

-parasympathetic and sympathetic ganglionic synapses (Nn) -NMJ/ skeletal muscle: (Nm)

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4
Q

Where are muscarinic receptors located?

A

-parasympathetic end organs (Ach)-sympathetic input to sweat glands

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5
Q

Iris sphincter vs dilator: (shape)

A

sphincter- circular muscle dilator- radial

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6
Q

Describe the process of accomodation:

A

-near stimulus -contracture of ciliary muscle -loosening of the zonules -thickening of lens

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7
Q

Define: cycloplegia

A

paralysis of ciliary muscle= inability to accomodate

stimuli spasm of accomodation: overstimulation of ciliary muscle/ chronic accomodation= blurring, pain

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8
Q

Function of the aqeuous humor

A

-nutrients -mechanical stability/ provides healthy IOP

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9
Q

Normal tension glaucoma:

A

glaucoma in the presence of normal intraocular pressure

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10
Q

“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.

A

8-20 mmHg

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11
Q

1-3rd order sympathetic innervation of the eye:

A

1: hypothalamus –> ciliospinal center of budge (C8-T2)
2: sympathetic chain –> superior cervical ganglion
3: axons ride cartoids to targets

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12
Q

What sympathetic axons travel along ECA? ICA?

A

ECA: sweat glands of face below forehead
ICA: others (muller, dilator, sweat glands forehead)

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13
Q

Parasympathetic innervation of the eye?

A

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)

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14
Q

Iris dilator: main receptor:

A

a1

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15
Q

muellers muscle: main receptor:

A

a1

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16
Q

ciliary process: main receptor:

A

mainly B2 *some B1, a2

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17
Q

conjunctival blood vessels: main receptor:

A

a1

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18
Q

ciliary muscle/ iris sphincter: main receptor

A

muscarinic

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19
Q

Lacrimal gland: main receptor

A

a1

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20
Q

Rank relative % of all ophthalmic meds administered via each ROAs (6)

A

topical > intravitreal / retrobulbar > subtenton > oral > IV

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21
Q

Phenylephrine:
MOA
Use (3 ophtho use, 1 general use) general side effects?
3 ophtho ADRS

A

a1 agonist

  1. induces mydriasis for fundoscopic exam
  2. vasoconstriction (2.5%) = can differentiate scleritis from episcleritis
  3. separate iris from lens when stuck together (synechia, seen in uveitis) (10%)
  4. nasal decongestion Optho

ADRs:-a1 systemic effects + lid retraction, lacrimation, angle closure in eye

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22
Q

Epinephrine historical use in ophtho:

A

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

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23
Q

Why isn’t epinephrine effective for mydriasis/ fundoscopic exam?

A

melanin of iris binds epi (inhibits its action on pupillary muscles)
*results in Iris/Lens pigmentation from Epi deposits

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24
Q

Most dangerous effects of epinephrine on the eye? (3)

A
  • increased IOP-angle closure= EMERGENCY
  • cystoid macular edema: decreased acuity/ possibly
  • PERMANENT VISION LOSS
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25
Q

Even in the presence of phenylephrine, accomodation + light reflex can still occur. Why? How is this blocked for surgeries/ exams?

A

-parasympathetic system still intact! * ciliary muscle and iris sphincter have largely muscarinic receptors (few a1, so phenylephrine does not block) * must co-administer anticholinergic

26
Q

Apracyclonidine:

  • MOA & drug it is derived froM
  • Most common ophtho use
  • ocular side effects
A

-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

27
Q

3 ways that apracyclodine may treat increased IOP:

A

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

28
Q

Why isnt apracyclodine used to chronically treat glaucoma?

A

significant drift/ loss of efficacy over time; only use to emergently decrease IOP

29
Q 
Brimonidine
MOA
**First line treatment for: 
-2nd line treatment for: 
-Allergic potential
-Side effects
A
  • 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)
30
Q

Open angle glaucoma first line treatments: (2 general categories)

A

B blockers and prostaglandins

31
Q

How is brimonidine “neuroprotective” to the optic nerve?

A

a2 stimulation- vasodilation- increased blood supply to CN2

32
Q

**What condition is cocaine used to diagnose? How?What concentration is used?

A

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%

33
Q

Hydroxyamphetamine MOA + What condition is it used to diagnose? How?

A
  • 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
34
Q

Causes of pre-ganglionic Horner’s? (3)

A

1- tumor at apex of lung (Pancoasts)
2- thoracic aortic aneurysm
3- carotid endarterectomy

35
Q

Causes of post- ganglionic Horner’s (2)

A

1-goiter

2-cavernous sinus syndrome

36
Q

Dapiprazole: MOAUse ADR (2)Still Used?

A

MOA: a-block
Tx: reverses clinically (phenylephrine) induced dilation
ADR: hyperemia of conjunctival vessels, ptosis
*no longer used because short shelf life and $$$

37
Q 
Timolol 
MOA 
**Use (Gold Standard For?) 
Dosing? 
Benefits? (3) 
Don't give it to who?
A
  • 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**
38
Q

What are levobunolol and metipranolol?

A

Derivatives of timolol

-levobutol has longer duration of action than timolol

39
Q

Contraindications to use of timolol, levobunol, or metipranolol? Optho related ADRs?

A
  • COPD/ asthma/bronchitis (B2 block)
  • CHF

-ADR: minimal, some corneal anesthesia

40
Q

Betaxolol:
MOA
Use

A
  • selective B1 block
  • treats glaucoma safely in patients with COPD/ Asthma (“Bettah 1, makes breathing less TAXing”)
  • Still contraindicated in CHF
41
Q

Cartelol:
MOA
Use
**Special because?

A

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

42
Q

Rank ophtho B blocks in terms of potency

A

cartelol >timolol/levobunolol>betaxol > metipranolol

43
Q

Use for all B blockers in ophtho?

A

glaucoma treatment decreases AH output from ciliary processes by blocking B receptors (B2»>)
(Decrease Adenylate Cyclase/ cAMP pathway activity)

44
Q

Three drugs that may induce miosis/ reduce IOP?
What is their class/action?
What is their ROA?

A

cholinergic agonists

pilocarpine- topical
acetylcholine/ carbachol- injections

45
Q

**Pilocarpine important use?

Two special characteristics (Duration of action? metabolism?)

A
  • 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
46
Q

Pilocarpine-ADRs (general trend + 2 important systemic): ADRs 2 ophtho:

A

Systemic: SLUDE BBB + pulmonary edema and mental status change
Optho: accommodation spasm (under 40yrs) + miosis (dimming of vision/ restricted peripheral vision)

47
Q

When is acetylcholine used and why is it rare?

A

intraocular injection for some surgeries

quickly metabolized by AchE so miosis effects are very short lasting

48
Q

When is carbachol used?

important consideration?

A

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

49
Q

Physostigmine and neostigmine:
MOA
When are they used ?

A

AchEi

short acting used to rescue from acute angle closure glaucoma if patient is ALLERGIC to pilocarpine (rare)

50
Q

Echothiopate and Isofluorophate:
MOA
Why not used ?

A 
Organic AchEi (phosphorylates the enzyme)=IRREVERSIBLE
 ***severe ADRs (^^^SLUDE BBB + retinal detachment, cataracts, iris cysts etc)
51
Q

Four uses for cholinergic antagonists?

A
  1. mydriasis
  2. cycloplegia (ciliary muscle inhibition- gets rid of accomodation for surgery)
  3. Accommodative Esotropia (infants + kiddos)
  4. uveitis/ inflammation- relieve pain, decrease risk posterior synechia to lens
52
Q 
Tropicamide:
MOA 
Use (combined with?) 
Not good for? 
Safe for?
A

anti-cholinergic

  • mydriasis/Retinal Exam
  • combined with phenylephrine
  • Not good for cycloplegia- inhibits light, but not accommodation response
  • Safe for Glaucoma Pt
53
Q

cyclopentolate:
MOA
Use for

A

anticholingeric mydriasis + cycloplegia

*SURGERY because long lasting + loss of accomodation (not comfortable for patient during standard exam)

54
Q

Homatropine:
MOA
Use

A

anti-cholinergic
mydriasis + cycloplegia
PAIN RELIEF (uveitis)

effects last even longer than cyclopentolate
*reduces amount of inflammatory modulators
mechanically forced from vessels during contraction

55
Q

Atropine
MOA
Use in ophtho (2)
*****Avoid in what two populations?

A

anti-cholinergic EXTREME cycloplegia and mydriasis

  1. Exam for infants/ children
  2. Treats accommodative esotropia in children

*****Down syndrome or Glaucoma

56
Q

What is accommodative esotropia?

Why is atropine effective treatment?

A

Disease causes eye to turn inward because of excess accommodation (stimulating convergence)
*Atropine causes cycloplegia (prevents accomodation)

57
Q

Which anti-cholinergic is most contraindicated in glaucoma?

Which is safe for glaucoma?

A

atropine= serious effects

tropicamide has low efficacy and is safe in glaucoma

58
Q

Rate length of mydriasis/cycloplegia for each of the four anti-cholinergics?

A

atropine > homatropine > cyclopentolate > tropicamide atropine = 288 hours- 12 DAYS

59
Q

Rate amount of mydriasis achieved for each of the four anti-cholinergics?

A

atropine > tropicamide> cyclopentolate > homatropine

60
Q

Which anti-cholinergic requires the highest concentration for effect?

A

homatropine(5%) - all others need 1%

61
Q

How to diagnose parasympathetic damage to eye? (Blown pupil)

A

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
62
Q

How long does it take for tropicamine to reach max mydriasis?
how long does mydriasis last?

A

20-30 min

4 hours

Neuro-Psych Exam II (11 decks)

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