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Friedman's Ophthalmology > Pharmacology > Flashcards

Pharmacology Flashcards

(90 cards)

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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
Name the dry eye insert of hydroxypropyl cellulose
Artificial tear slow release pellet
26
What is a collagen shield used for?
bandage contact lens pre-soaked in antibiotics
27
What are the advantages of subconjunctival/subtenon's drug administration?
* increases duration and concentration * bypasses conjunctival and corneal barriers * avoids systemic toxicity * useful if poor compliance
28
What is the mechanism by which anesthetics work?
reversable blockade of nerve fiber conduction (blocks sodium channels)
29
What state makes anesthetic less effective?
anesthetics are pH dependent (less effective at low pH (inflammed tissue))
30
What are the 2 types of anesthetics?
* Esters * Amides
31
What enzyme hydrolyzes esters? where are they metabolized? Name some examples
* hydrolyzed by plasma cholinesterase * metabolized in the liver * cocaine, tetracaine, proparicaine, benoxinate
32
What are 2 advantages of amide anesthetics?
longer duration, less systemic toxicity
33
Where are amides metabolized?
the liver
34
Name some examples of amides?
Lidocaine, mupivicaine, bupivicaine
35
How do topical anesthetics increase permeability to the cornea?
Disturb intercellular juctions in the corneal epithelium
36
What is the duration og Proparicaine (ophthaine)?
10-30 min
37
What are some of the negative side effects of proparacaine?
* corneal toxicity * may cause allergic dermatitis (also common with atropine and neomycin) * does not necessarily have cross reactivity with teracaine
38
What are the differences between proparacaine and Tetracaine?
Tetracaine is similar to proparacaine but longer duration (2-3 hours) and more toxic to corneal epithelium
39
what is benoxinate?
* similar to proparacaine * Combined with fluoroscein for tonometry (Fluress)
40
What is cocaine used for in ophthalmology?
* sympathomimetic effect (Horner's syndrome) * Excellent anesthesia * high epithelial toxicity
41
Why do you combine anesthetics (like lidocaine) with epinephrine?
epi (1:100,000) is used to increase duration yb preventing systemic absorption Also decreases bleeding
42
What medication can be combined with lidocaine to increase tissue pentration?
hyaluonidase (Wydase) 150IU increases tissue penetration, but decreases duration
43
What are the major side effects of retrobulbar anesthesia?
* respiratory depression * bradycardia
44
What is the duration of lidocaine (xylocaine)?
1-hour duration, 2 hours with epinephrine
45
What is the duration of action of procaine (novocaine)?
30-45 min duration
46
What is the duration of action of mepivacaine (carbocaine)?
2-hour duration
47
What is the duration of action of Bupivicaine (Marcaine)?
6-hour duration
48
What is the effect of anesthetics on IOP?
all agents decrease IOP except ketamine, chloral hydrate, N20, and ether
49
What is the inheritance pattern of malignant hyperthermia?
rarea autosomal dominant
50
Exposure to which inhalation agents can induce malignant hyperthermia?
* most commonly halothane * Also succhinylcholine and haloperidol
51
Which populations are more commonly effected by malignant hyperthermia?
most common in children and males
52
What is malignant hyperthermia thought to be due to?
* calcium binding disorder in sarcoplasmic reticulum that causes increased intracellular calcium which then stimulates muscle contraction * interference with oxidative phosphorylation causes hypermetabolic crisis
53
54
What is the common genetic mutation in patients succeptible to malignant hyperthermia?
Most have a defect in ryanidine receptor (RYR-1 gene on chomosome 19q13.1)
55
What is the first sign of malignant hyperthermia?
tachycardia
56
What are other early signs of malignant hyperthermia?
* elevated CO2 levels * tachypnea * unstable BP * arrythmias * cyanosis * sweatingmuscle rigidity (trismus from masseter rigidity)
57
What are the late signs of malignant hyperthermia?
* Increased temperature * heart failure * DIC (disseminated intravascular coagulation) *
58
What do the lab tests show for malignant hyperthermia?
* Respiratory and metabolic acidosis * increased K, Mg, myoglbin, creatine phosphokinase * hypoxemia * hypercarbia * myoglobinuria
59
What lab tests are used to confirm diagnosis of malignant hyperthermia?
* elevated creatinine phosphokinase * muscle biopsy/ contracture test * platelet bio assay (decreased ATP in platelet expoured to halothane)
60
How do you treat malignant hyperthermia?
61
What is the prognosis of malignant hyperthermia?
\<5% mortality
62
What is the effect of the sympathetic nervous system on the following organs/function?
63
What is the effect of the parasympathetic nervous system on the following organs/functions?
64
Where does the sympathetic nervous system synpase in the spinal column?
Synapses near the cord (superior cervical ganglion)
65
What is the function of alpha-1 adrenergic receptors?
* smooth muscle contraction (arteries (decrease aqueous production by reducing ciliary body blood flow)) * iris dilator * Muller's muscle
66
What is the functions of alpha-2 adrenergic receptors?
* feedback inhibition * ciliary body (decreases production and/or increases outflow)
67
What is the function of beta-1 adrenergic receptors?
* Cardiac stimulation
68
what is the function of beta-2 adrenergic receptors?
* pulmonary, GI smooth muscle relaxation * ciliary body/trabecular meshwork (increase aqueous production, increase outflow facility)
69
What are the neurotransmitters of the sympathetic nervous system (pre-ganglionic and post ganglionic)
* acetylcholine (ACh) ater preganglionic terminal * epinephrine and norepinephrine at post ganglionic terminal
70
What is the enzyme that breaks down norepinephrine in the nerve terminal?
Mono-amine oxidase
71
What medications should be avoided when a patient is on an MAO inhibitor?
* cold remedies that contain epinephrine, phenylephrine, pseudoephedrine
72
What enzyme breaks down norepinephrine in the effector cell?
Catechol- O-methyltransferase
73
What medication prevents the storage of norepinephrine in the nerve terminal?
Reserpine
74
What drugs block the re-uptake of norepinephrine in the nerve terminal thus poteniating tnerve action)
* cocaine * tricyclic ant-depressants
75
What medication increases the release of norepinephrine from the nerve terminal?
Hydroxamphetamine
76
Where are the synapses of the parasympathetic nervous system?
Synapses near the end organ (ciliary ganglion)
77
Which postganlionic nerves are sympathetic vs parasympathetic?
* long postganglionic nerves = sympathetic * short postganglionic nerves = parasympathetic
78
Name the 2 types of cholinergic receptors in the parasympathetic nervous system
* niotinic * muscarinic
79
In what muscle types are nicotinic receptors found?
* somatic motor andpreganglionic utonomic nerves * (extraocular muscles, levator, orbicularis) * (outside the eye)
80
In what muscle types are muscarinic receptors found?
* postganglionic parasympathetic nerves * (iris sphincter, ciliary muscle) * (inside the eye)
81
What is the neurotransmitter of the parasympathetic nervous system?
Acetylcholine
82
What is the enzyme that breaks down acetylcholine?
Acetylcholinesterase
83
Name 3 direct acting agonists
* miochol (ACh) * carbachol * pilocarpine
84
Where do direct acting agonists act on the end organ or the nerve?
end organ (they do not need intact innervation)
85
What are some of the effects of direct acting agonists (like pilocarpine)?
* shallowing of the AC * disruption of blood aqueous barrier (think flare) * miosis * brow ache * decreased IOP
86
How long does miochol (ACh) last?
* very short acting (unstable) * 20 minutes of miosis when used intracamerally)
87
How long does carbochol (miostat) last?
8 hours
88
What is unique about pilocarpine compared to ACh?
* less potent than ACh * resistant to AChE * no miosis if IOP \>40mmHg
89
90
How do indirect acting agonists work to decrease IOP and cause miosis?
contract longtudinal fibers of ciliary muscle = increased outflow of rabecular meshwork

Friedman's Ophthalmology (12 decks)

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