Mydriatics And Cycloplegics Flashcards

1
Q

Autonomic: parasympathetic pathway to the iris

A

Pretectal n. -> EW n. -> ciliary ganglion -> sphincter

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2
Q

Autonomic, sympathetic pathway to the iris

A

Hypothalamus -> ciliospinal center of Budge -> superior cervical ganglion -> dilator muscle

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3
Q

Direct agonist

A

A substance that binds to and fully activates its neuronal receptor
(Drug acts as a NT)

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4
Q

Indirect agonist

A

Potentials the action of the neurotransmitter

Causing NT to bind

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5
Q

Antagonist

A

Any substance that inhibits the activity of the neurotransmitter

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6
Q

An antagonist may bind to __ but not activate it.

A

Bond to a receptor

Affinity but no efficacy

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7
Q

An antagonist may bind to ___ , thereby deactivating it.

A

Neurotransmitter

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8
Q

Cholinergic agents mimic

A

Acetylcholine

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9
Q

Acetylcholinerase

A

Degrades ACh and halts transmission

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10
Q

Muscarinic

A

ACh receptors present in the ciliary body’s and iris

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11
Q

Nicotinic

A

ACh receptors are present in somatic muscle

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12
Q

Muscarinic agonists bind to and activates

A

Cholinergic receptors

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13
Q

Muscarinic agonist drugs cause iris

A

Sphincter contraction leading to pupillary miosis

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14
Q

Muscarinic agonist causes ciliary body

A

Contraction leading to accommodation

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15
Q

Example of a muscarinic agonist

A

Pilocarpine, green cap

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16
Q

Muscarinic antagonist binds to and inhibits

A

Cholinergic receptors (antimuscarinic)

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17
Q

Muscarinic antagonist causes pupil

A

Sphincter inhibition leading to mydryasis

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18
Q

Muscarinic antagonist causes ciliary body

A

Inhibition leading to Cycloplegia

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19
Q

Examples of muscarinic antagonist:

STopACH

A
Scopolamine 
Tropicamide 
Atropine 
Cyclopentolate 
Homatropine  
(Red cap)
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20
Q

All Mydriatics/ cycloplegic drugs are classified by the FDA as pregnancy category___ meaning….

A

Category C

Potential benefits may warrant use of the drug in pregnant women despite potential risks

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21
Q

CNS side effects caused by antimuscarinic agents vary depending on

A

The ability of the drug to penetrate the blood- brain barrier

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22
Q

Potential CNS side effects of antimuscarinic drugs include

A

Drowsiness, hallucinations, cognitive impairment, and coma

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23
Q

Atropine is the most

A

Potent and longest acting anti cholinergic available for clinical use

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24
Q

Atropine is only used when

A

Total cycloplegia is required

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25
Q

Residual accommodation is

A

The amount the patient is able to accommodate at the time of maximal cycloplegia

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26
Q

Residual accommodation of atropine

A

Zero diopters

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27
Q

What are the clinical uses of atropine?

A

Refraction, myopia control, amblyopia, uveitis

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28
Q

How is atropine used for refraction

A

Evaluation of esotropia in children less than 6 yrs ole

Duration of action too long for routine refraction

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29
Q

Atropine in myopia control

A

Long term low dose therapy inhibit progression

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30
Q

Atropine used in amblyopia

A

Penalization of better seeing eye as alternative to occlusion

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31
Q

Atropine used in uveitis

A

Long term relaxation of ciliary body in severe anterior uveitis

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32
Q

Contraindications and precautions of atropine

A

Allergy
Down’s syndrome
small children
Spastic paralysis or brain damage

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33
Q

What happens if atropine is given to spastic paralysis or brain damage

A

Increased risk of CNS effects and death in pts

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34
Q

Systemic overdose symptoms of atropine

A

Hot as a hare, blind as a bat, dry as a bone, red as a beet, mad as a hatter

Fever, blurred vision,, dry skin, flushing, delirium (hallucinations and psychosis)

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35
Q

Adverse effects of atropine

A

Effects from systemic overdose, and IOP elevation

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36
Q

Atropine causes open glaucoma pts to experience a transient increase in IOP because

A

Decreased tension on the scleral spur by the ciliary body will tend to shrink the aqueous drainage passages through the trabecular mesh work

The elevation of IOP is NOT due to angle closure

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37
Q

Relaxation of the ciliary muscle

A

Increases IOP

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38
Q

Contraction of the ciliary muscle

A

Decreases IOP

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39
Q

IOP effect of cycloplegic agents in normal patients

A

Minimal and variable

Iop might increase slightly

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40
Q

IOP effect of cycloplegic agents in subjects with POAG

A

IOP will increase following cycloplegia

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41
Q

Cyclopentolate is the drug of choice for

A

Routine cycloplegic refraction

Mostly used in 1%

42
Q

Typical residual accommodation of cyclopentolate is

A

1.25 D

43
Q

Using cyclopentolate, you will see faster cycloplegia with less residual accommodation in

A

Lightly pigmented eyes

44
Q

Pigment sequestration

A

Some drugs when instilled into the eye will reversible bind to melanin

45
Q

What happens if pigment sequestration occurs when a drug is instilled

A

While bound to melanin the drug is not available to induce any pharmacological effects

The drug will have a normal effect after being released fro melanin

46
Q

The net effect of pigment sequestration is

A

Delayed onset, prolonged duration of action and smaller peak pharmacological effect

47
Q

Pigment sequestration is most pronounced in

A

Heavily pigmented eyes

48
Q

Side effects of cyclopentolate

A

Stinging
Toxic keratitis with prolonged use
Transient elevation in IOP in POAG patients
DOSE RELATED CNS EFFECTS: TRANSIENT PSYCHOTIC REACTIONS MAY OCCUR BC IT READILY CROSSES BLODD BRAIN BARRIER

49
Q

Contraindications of cyclopentolate

A

Increased risk of CNS effects in infants, young children and children with spastic paralysis and brain damage

50
Q

Drug of choice for routine mydriasis

A

Tropicamide 0.5% and 1% sol.

51
Q

Whats the difference for 0.5% and 1% tropicamide

A

Equivalent mydriatic effect of 0.5% and 1%, greater cycloplegia with 1% solution

52
Q

Tropicamide is a clinically effective cycloplegia because

A

It lasts about 30 min

53
Q

Duration of action of tropicamide

A

Max mydriasis 20-30 min duration 6 hrs

Max cycloplegia 20-45 min duration 6 hrs

54
Q

Contraindications of tropicamide

A

No reported adverse systemic effects

Extremely safe systemically

55
Q

Side effects of tropicamide

A

Stinging upon instillation

Transient increase IOP in POAG patients

56
Q

Clinical considerations of homatropine

A

Weak but prolonged cycloplegic effect and strong mydriatic effect make it suitable for uveitis therapy

57
Q

Duration of action of homatropine

A

Max mydriasis 40-60 min duration 1-3 days

Max cycloplegia 30-60 min duration 1-3 days

58
Q

Contraindications of homatropine

A

Same as atropine :

Hypersensitivity, Down’s syndrome

59
Q

Clinical considerations of scopolamine

A

Not routinely used

Reserved for pts allergic to the others

60
Q

Duration of scopolamine

A

Very long
Max mydriasis 20-30 min duration 3-7 days
Max cycloplegia 30-60 min duration 3-7 days

61
Q

Contraindications of scopolamine

A

CNS effects are more common than other agents because it more easily crosses the blood brain barrier

62
Q

Cycloplegic refraction advantages (3)

A

More accurate refraction in kids and pts who are unable to cooperate

Diagnosis of accommodative esotropia and evaluating strabismus in kids

Necessary to diagnose latent hyperopia and pseudomyopia (acc spasm)

63
Q

Cycloplegic refraction disadvantages (4)

A

Decrease VAs because if spherical aberration

Loss of normal ciliary tonus lead as to refraction thats too hyperopic

Blurry vision and photophobia

Risk of adverse drug effects

64
Q

Cycloplegic refraction can lead to a refraction that is too hyperopic so you will need to

A

Cut plus from the refraction prior to prescription

65
Q

Tropicamide during cycloplegic refraction

Effectiveness decreases after____. Useful for ____patients.

A

Effectiveness decreases after 35 min

Useful for non amblyopia, non strabismus, myopic, or low hyperopic kids and adults

66
Q

Cyclopentolate for cycloplegic refraction

A

Drug of choice for cycloplegic refraction

67
Q

Atropine during cycloplegic refraction is used for ____.

A

Use in esotropia children < 6 years

Can reveal additional hyperopia in these children compares to cyclopentolate

68
Q

When will cycloplegic refraction be unreliable

A

If residual accommodation is >2.00D

69
Q

Using pupillary reactions to asses redisual accommodation

A

NOT RELIABLE

70
Q

Assessment of residual accommodation during cycloplegic refraction

A

Subjective push up of accommodative target ‘

Stability of Retinoscopy reflex

71
Q

Adrenergic neurotransmitter

A

Norepinephrine

72
Q

Transmitter uptake stops

A

Transmission

73
Q

What type of agonist/anti agonist is phenylephrine

A

Direct acting agonist

74
Q

Substance that increases the activity of the neurotransmitter

A

Indirect acting agonist

75
Q

Indirect acting agonist have 2 methods (and examples)

A
  1. Inhibit reputable of norepinephrine (cocaine)

2. Release of stored presypnaptic norepinephrine (hydroxyamphetamine)

76
Q

Direct alpha-Adrenergic agonist bind to

A

And activate alpha Adrenergic receptors

77
Q

Direct alpha Adrenergic agonist effect on eye (iris and ciliary body)

A

Causes stimulation of iris dilator muscle -> mydriasis

But no effect on ciliary body or accommodation -> no cycloplegia

78
Q

An example of a direct alpha Adrenergic agonist (mydriasis but no cycloplegia)

A

Phenylephrine (red cap)

79
Q

Mode of action of indirect alpha - Adrenergic agonist

A

Causes release of stored norepinephrine from the presypnaptic neuron

80
Q

Mydriatic effect of indirect alpha Adrenergic agonist

A

Same as direct

Stimulation of iris dilator - mydriasis

81
Q

An example of a indirect alpha Adrenergic agonist

A

Hydroxyamphetamine (red cap)

82
Q

Phenylephrine cardiovascular effects

A

Risk of adverse cardiovascular event have been more frequently reported with the 10% strength

Therefore 2.5% is recommended for routine use

83
Q

10% phenylephrine solution increases

A

10% strength produces an increase in rate but not magnitude of mydriasis

84
Q

10% strength of phenylephrine useful for

A

Breaking posterior Synechia

85
Q

% of phenylephrine used in clinic

A

2.5%

86
Q

Drug contraindications of phenylephrine

A

MAO inhibitors
Tricyclics antidepressants
Reserpine, guanthidine or methyldopa

87
Q

Avoid phenylephrine in patients who

A

Patients taking systemic antropine
Orthostatic hypotension
Malignant hypertension
Thyrotoxicosis

88
Q

Limit 10% strength phenylephrine to _________ when attempting to break synechia

A

Limit 10% strength to 1gtt per hour per eye when attempting to break synechia

89
Q

Do not give multiple doses of 2.5% sol for _____

A

routine dilation

Only recommended in infants and the elderly

90
Q

Phenylephrine systemic side effects

A

Acute systemic hypertension ventricular arrhythmia, tachycardia, subarachnoid hemorrhage

91
Q

Deaths following phenylephrine

A

Following use of 10% topical phenylephrine have been reported

92
Q

Ocular side effects of phenylephrine

A

Mild stinging, pigmented aqueous floaters, little or no effect on IOP

93
Q

Use of 10% phenylephrine for routine dilation

A

NEVER

Only used for breaking posterior synechia

94
Q

When to use multiple doses of phenylephrine

A

NEVER for routine pupil dilation

If patient isn’t dilating , instill additional drops of tropicamide, not phenylephrine

95
Q

Hydroxyamphetamine clinical considerations

A

Mydriatic effectiveness equivalent to phenylephrine

Role in localizing lesions in Horner syndrome

Only commercially available as 1% solution combine with 0.25% tropicamide

96
Q

Localizing lesion in Horner syndrome

A

Hydroxyamphetamine

97
Q

Duration of action hydroxyamphetamine

A

Max mydriasis 60 min

Duration 6 hrs

98
Q

Side effects of hydroxyamphetamine

A

Little to no elevation of IOP in POAG pts

Less stinging than phenylephrine

99
Q

Safety difference between hydroxyamphetamine and phenylephrine

A

May be safer than phenylephrine in high risk pts. However, cardiovascular events have occurred shortly following paremyd instillation

100
Q

Hydroxyamphetamine can be used in the differential diagnosis of

A

Horner syndrome

Indirect alpha Adrenergic agonist

101
Q

Hydroxyamphetamine causes

A

Release of norepinephrine from the presypnaptic neuron

If presypnaptic neuron is dead -> no dilation in response to hydroxyamphetamine