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Friedman's Ophthalmology > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What is pharmacodynamics?

A

the study of biochemical and physiologic effects of drugs and their mechanisms of action.

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2
Q

What is pharmacokinetics?

A

the study of the factors that determine the relationship between the drug doseage and the change in concentration over time in a biological system

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3
Q

What is bioavailability?

A

Amount of drug available (pentration into ocular tissues)

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4
Q

What factors does the bioavailbility depend on?

A
  • concentration
  • rate of absorption
  • tissue binding
  • transport
  • metabolism
  • excretion
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5
Q

How can you change bioavailability by changing concentration?

A

Increase concentration:

limited by solubility and tonicity (hypertonicity causes reflex tearing which dilutes and washes drug from the eye)

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6
Q

How can you change bioavailability by using surfactants?

A

surface-active agents alter cell membranes, increasing permeability of corneal epithelium

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7
Q

How do you change bioavailability by using osmotics?

A

osmotics alter tonicity

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8
Q

How do you change bioavailability by changing pH?

A

Increase pH:

increases non-ionized (lipid soluable) form of drug, increasing corneal penetration (pH of tears = 7.4)

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9
Q

How do you change bioavailability by changing viscosity?

A

Increase viscosity:

Viscous additives (methylcellulose, polyvinyl alcohol) increase contact time and therefore penetration

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10
Q

How can you change the bioavailability by changing contact time?

A

Increase contact time:

gels and oil based ointment formulations (mineral oil, petrolatum)

polymer matrix (durasite) must be able to release drug.

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11
Q

What is therapeutic index?

A

a method of comparing potency of different antibiotics. A measure of relative effective (therapeutic) concentration of antibiotic at target site against a target organism

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12
Q

What is Inhibitory Quotient?

A

The most potent antibiotic has the lowest minimum inhibitory concentration (MIC) (or highest inhibitory quotient)

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13
Q

How many drops are in a bottle?

A

20-40 usually

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14
Q

How many uL can fit in the conjunctival cul-de-sac?

A

Holds only 10uL (20% of drop)

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15
Q

How much of a drop that I placed into the cul-de-sac is present 4 min later?

A

50% of drug (reflex tearing and normal tear turnover dilute drop)

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16
Q

What are the 2 barriers to corneal penetration of medications?

A
  • tight junctions
  • stroma
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17
Q

Where in the cornea are tight junctions present?

What type of drugs do they block?

A
  • epithelium and endothelium
  • limit passage of lipophilic drugs
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18
Q

Which drugs are blocked by the corneal stroma?

A

The stroma is water rich- it limits the passage of lipophilic drugs

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19
Q

Name 5 methods for increasing absorption of medications on th eyes

A
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20
Q

What is the prodrug of epinephrine?

A

propine

less toxicity

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21
Q

What is the prodrug of amfenac?

A

Nevanac (nepafenac)

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22
Q

Name 3 drugs that have better uptake in ointment form?

A
  • tetracyclines
  • chloramphenicol
  • fluorometholone
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23
Q

Which medication can be used as a sustained release gel on the ocular surface?

A

Pilocaripine (pilopine)

decreased dosing

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24
Q

Name the intraocular insert of pilocarpine.

over what period of time does it release?

A

Ocusert

membrane control system

slow release over 1 week

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25
Q

Name the dry eye insert of hydroxypropyl cellulose

A

Artificial tear slow release pellet

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26
Q

What is a collagen shield used for?

A

bandage contact lens pre-soaked in antibiotics

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27
Q

What are the advantages of subconjunctival/subtenon’s drug administration?

A
  • increases duration and concentration
  • bypasses conjunctival and corneal barriers
  • avoids systemic toxicity
  • useful if poor compliance
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28
Q

What is the mechanism by which anesthetics work?

A

reversable blockade of nerve fiber conduction

(blocks sodium channels)

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29
Q

What state makes anesthetic less effective?

A

anesthetics are pH dependent

(less effective at low pH (inflammed tissue))

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30
Q

What are the 2 types of anesthetics?

A
  • Esters
  • Amides
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31
Q

What enzyme hydrolyzes esters?

where are they metabolized?

Name some examples

A
  • hydrolyzed by plasma cholinesterase
  • metabolized in the liver
  • cocaine, tetracaine, proparicaine, benoxinate
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32
Q

What are 2 advantages of amide anesthetics?

A

longer duration, less systemic toxicity

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33
Q

Where are amides metabolized?

A

the liver

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34
Q

Name some examples of amides?

A

Lidocaine, mupivicaine, bupivicaine

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35
Q

How do topical anesthetics increase permeability to the cornea?

A

Disturb intercellular juctions in the corneal epithelium

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36
Q

What is the duration og Proparicaine (ophthaine)?

A

10-30 min

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37
Q

What are some of the negative side effects of proparacaine?

A
  • corneal toxicity
  • may cause allergic dermatitis (also common with atropine and neomycin)
  • does not necessarily have cross reactivity with teracaine
38
Q

What are the differences between proparacaine and Tetracaine?

A

Tetracaine is similar to proparacaine but longer duration (2-3 hours) and more toxic to corneal epithelium

39
Q

what is benoxinate?

A
  • similar to proparacaine
  • Combined with fluoroscein for tonometry (Fluress)
40
Q

What is cocaine used for in ophthalmology?

A
  • sympathomimetic effect (Horner’s syndrome)
  • Excellent anesthesia
  • high epithelial toxicity
41
Q

Why do you combine anesthetics (like lidocaine) with epinephrine?

A

epi (1:100,000) is used to increase duration yb preventing systemic absorption

Also decreases bleeding

42
Q

What medication can be combined with lidocaine to increase tissue pentration?

A

hyaluonidase (Wydase) 150IU increases tissue penetration, but decreases duration

43
Q

What are the major side effects of retrobulbar anesthesia?

A
  • respiratory depression
  • bradycardia
44
Q

What is the duration of lidocaine (xylocaine)?

A

1-hour duration, 2 hours with epinephrine

45
Q

What is the duration of action of procaine (novocaine)?

A

30-45 min duration

46
Q

What is the duration of action of mepivacaine (carbocaine)?

A

2-hour duration

47
Q

What is the duration of action of Bupivicaine (Marcaine)?

A

6-hour duration

48
Q

What is the effect of anesthetics on IOP?

A

all agents decrease IOP except ketamine, chloral hydrate, N20, and ether

49
Q

What is the inheritance pattern of malignant hyperthermia?

A

rarea autosomal dominant

50
Q

Exposure to which inhalation agents can induce malignant hyperthermia?

A
  • most commonly halothane
  • Also succhinylcholine and haloperidol
51
Q

Which populations are more commonly effected by malignant hyperthermia?

A

most common in children and males

52
Q

What is malignant hyperthermia thought to be due to?

A
  • calcium binding disorder in sarcoplasmic reticulum that causes increased intracellular calcium which then stimulates muscle contraction
  • interference with oxidative phosphorylation causes hypermetabolic crisis
53
Q
A
54
Q

What is the common genetic mutation in patients succeptible to malignant hyperthermia?

A

Most have a defect in ryanidine receptor (RYR-1 gene on chomosome 19q13.1)

55
Q

What is the first sign of malignant hyperthermia?

A

tachycardia

56
Q

What are other early signs of malignant hyperthermia?

A
  • elevated CO2 levels
  • tachypnea
  • unstable BP
  • arrythmias
  • cyanosis
  • sweatingmuscle rigidity (trismus from masseter rigidity)
57
Q

What are the late signs of malignant hyperthermia?

A
  • Increased temperature
  • heart failure
  • DIC (disseminated intravascular coagulation)
    *
58
Q

What do the lab tests show for malignant hyperthermia?

A
  • Respiratory and metabolic acidosis
  • increased K, Mg, myoglbin, creatine phosphokinase
  • hypoxemia
  • hypercarbia
  • myoglobinuria
59
Q

What lab tests are used to confirm diagnosis of malignant hyperthermia?

A
  • elevated creatinine phosphokinase
  • muscle biopsy/ contracture test
  • platelet bio assay (decreased ATP in platelet expoured to halothane)
60
Q

How do you treat malignant hyperthermia?

A
61
Q

What is the prognosis of malignant hyperthermia?

A

<5% mortality

62
Q

What is the effect of the sympathetic nervous system on the following organs/function?

A
63
Q

What is the effect of the parasympathetic nervous system on the following organs/functions?

A
64
Q

Where does the sympathetic nervous system synpase in the spinal column?

A

Synapses near the cord (superior cervical ganglion)

65
Q

What is the function of alpha-1 adrenergic receptors?

A
  • smooth muscle contraction (arteries (decrease aqueous production by reducing ciliary body blood flow))
  • iris dilator
  • Muller’s muscle
66
Q

What is the functions of alpha-2 adrenergic receptors?

A
  • feedback inhibition
  • ciliary body (decreases production and/or increases outflow)
67
Q

What is the function of beta-1 adrenergic receptors?

A
  • Cardiac stimulation
68
Q

what is the function of beta-2 adrenergic receptors?

A
  • pulmonary, GI smooth muscle relaxation
  • ciliary body/trabecular meshwork (increase aqueous production, increase outflow facility)
69
Q

What are the neurotransmitters of the sympathetic nervous system (pre-ganglionic and post ganglionic)

A
  • acetylcholine (ACh) ater preganglionic terminal
  • epinephrine and norepinephrine at post ganglionic terminal
70
Q

What is the enzyme that breaks down norepinephrine in the nerve terminal?

A

Mono-amine oxidase

71
Q

What medications should be avoided when a patient is on an MAO inhibitor?

A
  • cold remedies that contain epinephrine, phenylephrine, pseudoephedrine
72
Q

What enzyme breaks down norepinephrine in the effector cell?

A

Catechol- O-methyltransferase

73
Q

What medication prevents the storage of norepinephrine in the nerve terminal?

A

Reserpine

74
Q

What drugs block the re-uptake of norepinephrine in the nerve terminal thus poteniating tnerve action)

A
  • cocaine
  • tricyclic ant-depressants
75
Q

What medication increases the release of norepinephrine from the nerve terminal?

A

Hydroxamphetamine

76
Q

Where are the synapses of the parasympathetic nervous system?

A

Synapses near the end organ (ciliary ganglion)

77
Q

Which postganlionic nerves are sympathetic vs parasympathetic?

A
  • long postganglionic nerves = sympathetic
  • short postganglionic nerves = parasympathetic
78
Q

Name the 2 types of cholinergic receptors in the parasympathetic nervous system

A
  • niotinic
  • muscarinic
79
Q

In what muscle types are nicotinic receptors found?

A
  • somatic motor andpreganglionic utonomic nerves
  • (extraocular muscles, levator, orbicularis)
  • (outside the eye)
80
Q

In what muscle types are muscarinic receptors found?

A
  • postganglionic parasympathetic nerves
  • (iris sphincter, ciliary muscle)
  • (inside the eye)
81
Q

What is the neurotransmitter of the parasympathetic nervous system?

A

Acetylcholine

82
Q

What is the enzyme that breaks down acetylcholine?

A

Acetylcholinesterase

83
Q

Name 3 direct acting agonists

A
  • miochol (ACh)
  • carbachol
  • pilocarpine
84
Q

Where do direct acting agonists act on the end organ or the nerve?

A

end organ (they do not need intact innervation)

85
Q

What are some of the effects of direct acting agonists (like pilocarpine)?

A
  • shallowing of the AC
  • disruption of blood aqueous barrier (think flare)
  • miosis
  • brow ache
  • decreased IOP
86
Q

How long does miochol (ACh) last?

A
  • very short acting (unstable)
  • 20 minutes of miosis when used intracamerally)
87
Q

How long does carbochol (miostat) last?

A

8 hours

88
Q

What is unique about pilocarpine compared to ACh?

A
  • less potent than ACh
  • resistant to AChE
  • no miosis if IOP >40mmHg
89
Q
A
90
Q

How do indirect acting agonists work to decrease IOP and cause miosis?

A

contract longtudinal fibers of ciliary muscle = increased outflow of rabecular meshwork

Friedman's Ophthalmology (12 decks)

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