Term
|
Definition
| Stimulation of opiate receptors leads to G-protein coupled decrease in adenylate cyclase and a decrease in cAMP within the cell. This results in an increased K+ efflux and decreased Ca++ influx, leading to decreased neuronal excitability and decreased neurotransmitter release. |
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Term
|
Definition
| analgesic, (spinal supraspinal and peripheral) respiratory depressant, antidiarrheal, sedation, euphoria |
|
|
Term
|
Definition
| analgesic, antidiarrheal, diuresis, psychotomimesis, sedation |
|
|
Term
|
Definition
| analgesic, respiratory depressant, antidiarrheal |
|
|
Term
|
Definition
| Specific opiate receptor antagonists |
|
|
Term
|
Definition
| Specific opiate receptor antagonists |
|
|
Term
|
Definition
i. Orally effective
ii. Also parenterally
iii. 1/10th morphine potency, SC
iv. Codeine is metabolized to morphine which accounts for the analgesic actions
v. Frequently used in combination with Acetaminophen or ASA
vi. Effective for severe pain if injected, not orally
vii. All of morphine’s effects and toxicities when given in equal analgesic doses
viii. Used frequently for antitussive actions |
|
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Term
|
Definition
(1) Non-narcotic anti-tussive
(2) Dextroisomer of levomethorphan (levo is analgesic) (close to codeine)
(3) Probably acts on a non-Opioid receptor (not blocked by Naloxone) (maybe blocking NMDA receptors)
(4) Anti-tussive ability equivalent to codeine
(5) No respiratory depression, analgesia or euphoria
(6) Over-the-counter - Fairly safe – effective??
(7) Opiate dependence is not a problem |
|
|
Term
|
Definition
i. Five times more potent than morphine as an analgesic
ii. Faster onset and shorter duration |
|
|
Term
|
Definition
| Equal to morphine and orally effective |
|
|
Term
| Hydrocodone and Acetaminophen (Vicodin) |
|
Definition
| Simple addition of –OH group, otherwise the same as Oxycodone |
|
|
Term
Meperidine (Demerol)
pethidine |
|
Definition
i. Different structure – first completely synthetic
ii. More risk of convulsant effects (still need a high dose or other added agents)
iii. Available for IM, IV, and oral administration
iv. Used as an obstetric agent
v. Only used as an analgesic (less antitussive and antidiarrheal than others)
vi. About 1/10 to 1/5 the morphine potency with an equal efficacy for side effects (may be less spasmogenic – less colic)
vii. Easily crosses placenta and depresses respiration in fetus |
|
|
Term
| Diphenoxylate (with atropine = Lomotil) |
|
Definition
(a) Common anti-diarrheal
(b) Atropine added to decrease abuse
(c) Schedule 5 requires prescription |
|
|
Term
|
Definition
| is equal to diphenoxylate as an antidiarrheal, has a lower abuse potential and is available over the counter. Poor lipid solubility prevents CNS effects. |
|
|
Term
|
Definition
i. Different structure
ii. No obvious resemblance to morphine or meperidine
iii. Still excellent analgesic
iv. All the same actions and toxicities
v. Effective orally or injected
vi. Equal potency to morphine but longer duration in man after repeated doses
vii. Widely used as analgesic
viii. Also in opiate maintenance programs
ix. LAAM, l-alpha acetyl methadol, has three day duration of action |
|
|
Term
|
Definition
(1) Less potent than codeine
(2) Orally active
(3) Many opiate drawbacks without increased efficacy over aspirin
(4) Especially potent depression of respiration in combination with alcohol or CNS depressants
(5) withdrawn from US market in November 2010 |
|
|
Term
|
Definition
(1) Equal to morphine as an analgesic
(2) Much less abuse
(3) Blocks receptor in morphine dependent patients
(4) Agonist/Antagonist/Mixed
(5) Partial agonist at µ
(6) Weak antagonist at κ
(7) Search for analgesia without addiction |
|
|
Term
|
Definition
(1) Most frequently used of the mixed agonist/antagonists
(2) Weak antagonist at µ
(3) Good analgesia via κ receptor agonist activity
(4) Low addiction liability
(5) Less nausea and vomiting than morphine
(6) Good for chronic pain management
(7) ¼ to ½ morphine potency
(8) Subcutaneous or oral administration |
|
|
Term
|
Definition
(1) Newer analgesic with weak opiate mu-receptor agonist binding (as well as weak inhibition of NE & 5-HT uptake, so it also has antidepressant actions)
(2) An active metabolite may also have analgesic activity (mu)
(3) Can cause physical dependence, but very low abuse potential so not a schedule controlled substance.
(4) Toxicities include dizziness, vertigo, CNS stimulation, constipation, pruritus, GI upset, seizures |
|
|
Term
|
Definition
| Same as methadone but threedays |
|
|
Term
|
Definition
| Drug to take to help replace PGs in GI |
|
|
Term
|
Definition
| poor CNS penetration, mostly anti-inflammatory |
|
|
Term
|
Definition
a. Very popular analgesic/antipyretic
b. Good substitute for aspirin
c. No gastrointestinal problems
d. No increased uric acid (gout)
e. No platelet inhibition
f. No cross-sensitivity to aspirin
g. No Reye's syndrome risk
h. Except no anti-inflammation action
i. Very safe in therapeutic doses – rare allergies – rash etc
j. Method of action: weak inhibitor of cycloxygenase (different isozyme? COX – 3? Only in CNS?) |
|
|
Term
|
Definition
| cure fore acetaminophen OD helps glutathione prevents liver damage |
|
|
Term
|
Definition
i. Potency 10 to 40 times that of aspirin
ii. More frequent toxicities (35-50%), especially with long-term use, therefore used only as last resort type.
iii. Common toxicities include gastrointestinal and headache
(1) 20% must discontinue |
|
|
Term
|
Definition
Active metabolite - is more effective than parent
(2) Related to Indomethacin; less gastrointestinal toxicities |
|
|
Term
|
Definition
| Longer duration of action |
|
|
Term
|
Definition
Longer duration of action
Less GI toxicities |
|
|
Term
|
Definition
| Decreases free arachidonic acid Ands a SA |
|
|
Term
|
Definition
COX2 Selectivity
Anti-inflammatory mostly
Little action on GI and platelet aggregation
Sulfa alergies wont like this one
COX2 pulled off market b/c increase risk of thrombotic events,MI,Stroke |
|
|
Term
|
Definition
short acting 5-7 hours
regular insulin |
|
|
Term
|
Definition
Isophane insulin suspension
intermediate acting 18-24 hrs |
|
|
Term
|
Definition
Longest acting: 36hrs
provide basal levels throughout the day
can be comined with short term insuin for better glucose conrtol |
|
|
Term
|
Definition
Oral Hypoglycemics
. MOA –These agents can stimulate the release of insulin from functioning beta cells. Binding of the sulfonylureas to an ATP-dependent K+ channel leads to a decrease in K+ efflux and an increase in Ca++ influx, which gives greater insulin release upon stimulation by glucose. There is also an increased sensitivity of peripheral tissues to the actions of insulin, enhancing glucose uptake.
Sulfonylureas |
|
|
Term
Glipizide (Glucotrol)
b. Glyburide (Micronase)
c. Glimepiride (Amaryl) |
|
Definition
Oral Hypoglycemics
Sulfonylureas |
|
|
Term
|
Definition
Oral Hypoglycemics
Secretagogues |
|
|
Term
|
Definition
Oral Hypoglycemics
Secretagogues
MOA – stimulates insulin release from active beta cells through a similar MOA to the sulfonylureas – same channel binding site. |
|
|
Term
|
Definition
Antihyperglycemic agents
Biguanides
MOA is not clearly understood. May act by decreasing glucose output from the liver (decreasing gluconeogenesis), also increases insulin action (insulin sensitivity) on muscle and fat to increase uptake into cells (may simply be the lower blood glucose levels) |
|
|
Term
| acarbose (Glucobay) (Precose) |
|
Definition
Alpha-glucosidase inhibitors
MOA – inhibit GIT enzymes that breakdown complex carbohydrates thus they delay and reduce the amount of monosaccharides absorbed |
|
|
Term
|
Definition
Alpha-glucosidase inhibitors
MOA – inhibit GIT enzymes that breakdown complex carbohydrates thus they delay and reduce the amount of monosaccharides absorbed |
|
|
Term
|
Definition
Thiazolidinediones (glitazones)
MOA still unclear but may involve agonist-like action on PPAR receptors (peroxisome proliferator-activated receptor) which would increase gene transcription. This leads to increased uptake and utilization of glucose by the tissues and increases insulin sensitivity. Specific proteins; glut-4 (transporter for glucose), lipoprotein lipase, fatty acid transporter protein, and many others |
|
|
Term
|
Definition
Thiazolidinediones (glitazones)
MOA still unclear but may involve agonist-like action on PPAR receptors (peroxisome proliferator-activated receptor) which would increase gene transcription. This leads to increased uptake and utilization of glucose by the tissues and increases insulin sensitivity. Specific proteins; glut-4 (transporter for glucose), lipoprotein lipase, fatty acid transporter protein, and many others |
|
|
Term
|
Definition
MOA – a glucagon-like peptide 1 (GLP-1) receptor agonist which basically inhibits glucagon secretion, increases insulin secretion and delays gastric emptying. (incretin mimetic)
ii. given by subcutaneous injection (small peptide)
iii. toxicities – common
a) nausea
b) diarrhea
c) vomiting
. more serious – much less frequent
a) pancreatitis
b) possible thyroid carcinoma (liraglutide)
c) anaphylactic reactions (exenatide |
|
|
Term
|
Definition
MOA – a glucagon-like peptide 1 (GLP-1) receptor agonist which basically inhibits glucagon secretion, increases insulin secretion and delays gastric emptying. (incretin mimetic)
ii. given by subcutaneous injection (small peptide)
iii. toxicities – common
a) nausea
b) diarrhea
c) vomiting
. more serious – much less frequent
a) pancreatitis
b) possible thyroid carcinoma (liraglutide)
c) anaphylactic reactions (exenatide |
|
|
Term
|
Definition
| MOA – dipeptidyl peptidase 4 (DPP-4) inhibitors, which block the endogenous breakdown of GLP-1. Thus increasing the duration of incretin (GLP-1 and possibly others) actions to stimulate insulin release and inhibit glucagon release. |
|
|
Term
|
Definition
| MOA – dipeptidyl peptidase 4 (DPP-4) inhibitors, which block the endogenous breakdown of GLP-1. Thus increasing the duration of incretin (GLP-1 and possibly others) actions to stimulate insulin release and inhibit glucagon release. |
|
|
Term
|
Definition
| MOA – dipeptidyl peptidase 4 (DPP-4) inhibitors, which block the endogenous breakdown of GLP-1. Thus increasing the duration of incretin (GLP-1 and possibly others) actions to stimulate insulin release and inhibit glucagon release. |
|
|
Term
|
Definition
Alcaine (Alcon)
Ophthaine (Squibb)
Ophthetic (Allergan) |
|
|
Term
|
Definition
| preservative - increase absobption |
|
|
Term
|
Definition
- agonist - some selectivity for 2
- 2 - post-synaptic receptors - inhibit adenylate cyclase, decrease cAMP, decreased aqueous production, also see increased uveoscleral outflow |
|
|
Term
|
Definition
regular insulin (crystalline zinc or lispro)
short acting 5-7 hours |
|
|
Term
|
Definition
isophane insulin suspension (NPH)
intermediate acting 18-24 hours |
|
|
Term
| insulin glargine (Lantus) |
|
Definition
|
|
Term
|
Definition
Sulfonylureas
major benefit comes from increased sensitivity of the beta cells to glucose, thus leading to the increase in insulin release
Binding of the sulfonylureas to an ATP-dependent K+ channel leads to a decrease in K+ efflux and an increase in Ca++ influx, which gives grater insulin release upon stimulation by glucose. There is also an increased sensitivity of peripheral tissues to the actions of insulin, enhancing glucose uptakeToxicites:
3-60% depending on pt and drug
hypoglycemia (can be profound)
nausea
rash
blood disorders
jaundice
muscle weakness/ataxia
dizziness and mental confusion |
|
|
Term
|
Definition
Sulfonylureas
major benefit comes from increased sensitivity of the beta cells to glucose, thus leading to the increase in insulin release
Binding of the sulfonylureas to an ATP-dependent K+ channel leads to a decrease in K+ efflux and an increase in Ca++ influx, which gives grater insulin release upon stimulation by glucose. There is also an increased sensitivity of peripheral tissues to the actions of insulin, enhancing glucose uptakeToxicites:
3-60% depending on pt and drug
hypoglycemia (can be profound)
nausea
rash
blood disorders
jaundice
muscle weakness/ataxia
dizziness and mental confusion |
|
|
Term
|
Definition
Sulfonylureas
major benefit comes from increased sensitivity of the beta cells to glucose, thus leading to the increase in insulin release
Binding of the sulfonylureas to an ATP-dependent K+ channel leads to a decrease in K+ efflux and an increase in Ca++ influx, which gives grater insulin release upon stimulation by glucose. There is also an increased sensitivity of peripheral tissues to the actions of insulin, enhancing glucose uptakeToxicites:
3-60% depending on pt and drug
hypoglycemia (can be profound)
nausea
rash
blood disorders
jaundice
muscle weakness/ataxia
dizziness and mental confusion |
|
|
Term
|
Definition
Sulfonylureas
major benefit comes from increased sensitivity of the beta cells to glucose, thus leading to the increase in insulin release
Binding of the sulfonylureas to an ATP-dependent K+ channel leads to a decrease in K+ efflux and an increase in Ca++ influx, which gives grater insulin release upon stimulation by glucose. There is also an increased sensitivity of peripheral tissues to the actions of insulin, enhancing glucose uptakeToxicites:
3-60% depending on pt and drug
hypoglycemia (can be profound)
nausea
rash
blood disorders
jaundice
muscle weakness/ataxia
dizziness and mental confusion |
|
|
Term
|
Definition
Secretagogues
: also stimulates insulin release from active beta cells
Short duration, used only preprandially
Not sulfa drugs
Can cause:
Hypoglycemia
Nausea
Dyspepsia
diarrhea |
|
|
Term
|
Definition
Secretagogues
: also stimulates insulin release from active beta cells
Short duration, used only preprandially
Not sulfa drugs
Can cause:
Hypoglycemia
Nausea
Dyspepsia
diarrhea |
|
|
Term
|
Definition
Biguanides
: by inhibiting glucose absorption from GIT and may decrease glucose output form the liver, also increases insulin action (insulin sensitivity) on muscle and fat to increase uptake into cells (maysimply lower blood glucose levels
Increase in lactic acidosis, esp in pts with renal insufficiency
Also rarely: megoblastic anemia
Commonly: diarrhea, nausea, other GI symptoms |
|
|
Term
| Acarbose (Glucobay)(Precose) |
|
Definition
Inhibits GIT enzymes that breakdown complex carbohydrates
Delay and reduce the amt of monosaccharides absorbedFrequent GI disturbances, diarrhea, pain and gas |
|
|
Term
|
Definition
Inhibits GIT enzymes that breakdown complex carbohydrates
Delay and reduce the amt of monosaccharides absorbedFrequent GI disturbances, diarrhea, pain and gas |
|
|
Term
|
Definition
MOA: increasing sensitivity of insulin receptors –
Still unclear but may involve action on gene transcription
Significant but infrequent toxicities:
Hepatotoxicity, edema, congestive heart failure |
|
|
Term
|
Definition
MOA: increasing sensitivity of insulin receptors –
Still unclear but may involve action on gene transcription
Significant but infrequent toxicities:
Hepatotoxicity, edema, congestive heart failure |
|
|
Term
|
Definition
MOA – a glucagon-like peptide 1 (GLP-1) receptor agonist which basically inhibits glucagon secretion, increases insulin secretion and delays gastric emptying. (incretin mimetic)
ii. given by subcutaneous injection (small peptide)
iii. toxicities – common
a) nausea
b) diarrhea
c) vomiting
iv. more serious – much less frequent
a) pancreatitis
b) possible thyroid carcinoma (liraglutide)
c) anaphylactic reactions (exenatide) |
|
|
Term
|
Definition
MOA – a glucagon-like peptide 1 (GLP-1) receptor agonist which basically inhibits glucagon secretion, increases insulin secretion and delays gastric emptying. (incretin mimetic)
ii. given by subcutaneous injection (small peptide)
iii. toxicities – common
a) nausea
b) diarrhea
c) vomiting
iv. more serious – much less frequent
a) pancreatitis
b) possible thyroid carcinoma (liraglutide)
c) anaphylactic reactions (exenatide) |
|
|
Term
|
Definition
MOA – dipeptidyl peptidase 4 (DPP-4) inhibitors, which block the endogenous breakdown of GLP-1. Thus increasing the duration of incretin (GLP-1 and possibly others) actions to stimulate insulin release and inhibit glucagon release.
ii. toxicities – common
a) upper respiratory infection
b) nasopharyngitis
c) headache
iii. more serious toxicities
a) pancreatitis
b) hypersensitivity reactions |
|
|
Term
|
Definition
MOA – dipeptidyl peptidase 4 (DPP-4) inhibitors, which block the endogenous breakdown of GLP-1. Thus increasing the duration of incretin (GLP-1 and possibly others) actions to stimulate insulin release and inhibit glucagon release.
ii. toxicities – common
a) upper respiratory infection
b) nasopharyngitis
c) headache
iii. more serious toxicities
a) pancreatitis
b) hypersensitivity reactions |
|
|
Term
|
Definition
MOA – dipeptidyl peptidase 4 (DPP-4) inhibitors, which block the endogenous breakdown of GLP-1. Thus increasing the duration of incretin (GLP-1 and possibly others) actions to stimulate insulin release and inhibit glucagon release.
ii. toxicities – common
a) upper respiratory infection
b) nasopharyngitis
c) headache
iii. more serious toxicities
a) pancreatitis
b) hypersensitivity reactions |
|
|
Term
|
Definition
- vasoconstriction - 1:1000 topical-cutaneous 0.1%
conjunctival vasoconstriction begins with in minutes lasts less than 1 hour and may be followed by reactive hyperemia (especially with repeated administration - use a longer acting agent)
- 1:50,000 - 1:200,000 injected with LA
- mydriasis - not very effective
- glaucoma - open angle (only) – No longer used
Adrenergic Agents - Agonists
- mydriatic - 1 agonist
- antiglaucoma - 1, 2, and 2 agonists
- vasoconstrictor/decongestant - 1 agonist |
|
|
Term
| Phenylephrine (Neo-Synephrine) |
|
Definition
- agonist (mainly 1)
- 1/8% (OTC), 2.5% & 10% (Rx) ophthalmic solutions
- some burning and local irritation with 10% - less likely with lower %s
- can precipitate a narrow angle glaucoma attack
1. Clinical Uses
- decongestant - vasoconstriction
- mydriasis - most common adrenergic mydriatic
- maximum effects 60 min; recovery within 5-7 hours
- decreased effect in dark irrides
- counteracts miotics - use for examining open-angle glaucoma patient on miotics
- treat ptosis from sympathetic denervation
- diagnosis of Horner’s syndrome – not definitive – only accurate in 71% of eyes with Horner’s
- breaking posterior synechia - 10% - after LA
- treat miotic cysts from ACh-esterase inhibitor – b
add 2.5% phenylephrine to the Achase inhibitor
Toxicity
- contraindicated in Thyrotoxicosis,
coronary artery disease, hypertension
- drug interactions – Tricyclic antidepressants,
MAO inhibitors, and guanethidine, reserpine
- especially with 10% (deaths have occurred with it’s use)
- CNS stimulation, headache
- CV effects; hypertension, subarachnoid hemorrhage, ventricular arrhythmias, tachycardia, reflex bradycardia, blanching of the skin
Local/Ocular effects
- transient pain and excess lacrimation
- keratitis
- liberation of iris pigment - floaters, older patient with dark irides
- post-dilation miosis - older patient
- rebound congestion
- conjunctival hypoxia
- angle closure |
|
|
Term
| Apraclonidine (Iopidine) 0.5%, 1% |
|
Definition
- agonist - some selectivity for 2
- 2 - post-synaptic receptors - inhibit adenylate cyclase, decrease cAMP, decreased aqueous production, also see increased uveoscleral outflow
- % is approved for use with argon laser trabeculoplasty
- Long-term effect to reduce IOP - treat POAG - 0.5%
- Some use in diagnosis of Horner’s syndrome - 1% (Horner’s eye dilates)
- Adverse effects – allergic reactions 20-50%
- 1 stimulation
- mydriasis
- lid retraction
- conjunctival blanching
- systemic effects of dry mouth, fatigue, lethargy, headache, symptoms of head cold |
|
|
Term
|
Definition
Sympathomimetics
naphazoline is also available in combo with OTC antihistamines |
|
|
Term
|
Definition
- Highly selective 2 adrenergic receptor agonist
- Same MOA for antiglaucoma as Iopidine
- Decreased aqueous production, increased uveoscleral outflow, may be neuroprotective
- Side effects – most frequent – hyperemia, stinging, burning, blurred vision, FBS.
- allergic reactions 5 - 10% (less than apraclonidine)
- dry mouth, headache, fatigue, lethargy, or drowsiness |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
Hydroxyamphetamine
Paremyd
Paredrine |
|
Definition
product discontinued – compounding pharmacy?) Paremyd – 1% combo with Tropicamide, 0.25%
- indirect acting – stimulates release of NE, blocks reuptake and some inhibition of MAO
- 1% solution - mydriatic
- diagnosis of post-ganglionic SNS denervation (Horner’s syndrome – no dilation in post-ganglionic Horner’s lesion)
- onset and duration of action equivalent to phenylephrine
- seems to be less irritating and less likely to cause systemic toxicity - especially with drugs which deplete NE |
|
|
Term
|
Definition
indirect - block NE reuptake
- mydriasis, vasoconstriction, and anesthesia
- Horner’s diagnosis – 4 & 10% (Schedule II controlled substance) dilation is reduced or absent in Horner’s eye regardless of location of lesion |
|
|
Term
| Dapiprazole 0.5%, (Rev –Eyes) |
|
Definition
Adrenergic Antagonists
-blocker (discontinued in US in July 2012)
reverse phenylephrine mydriasis, also some actions on tropicamide induced mydriasis
toxicity - conjunctival hyperemia (80%), burning (50%), corneal edema, ptosis and lid edema and erythema also occur
- 0.5% solution better than pilocarpine since less risk of secondary pupil block angle closure |
|
|
Term
|
Definition
|
|
Term
| Metipranolol (Optipranolol) |
|
Definition
|
|
Term
|
Definition
|
|
Term
| Carteolol (Ocupress) 1% solution |
|
Definition
Intrinsic Sympathomimetic Activity (ISA) - non-selective
Partial B agonist |
|
|
Term
|
Definition
| (brimonidine 0.2% and timolol 0.5%) |
|
|
Term
|
Definition
| (dorzolamide 2.0% and timolol 0.5%) |
|
|
Term
|
Definition
direct acting
- antagonists - Atropine at muscarinic sites
- acetylcholinesterase (AChE)
- limited use - 1% intracameral injection (Miochol)
- miosis
- toxicity and contraindications rare |
|
|
Term
|
Definition
- not susceptible to AchE
- topical 1.5 and 3% - glaucoma
- side effects - ocular
- systemic-
Parasympathomimetic agents |
|
|
Term
|
Definition
most popular cholinergic agonist (miotic)
- Treat glaucoma (POAG) 1, 2, 4 and 6%
- Treat acute angle closure glaucoma (2%)
- not susceptible to AchE
- don’t use to reverse mydriasis
- muscarinic only, less ciliary contraction
- excellent miotic - used to break angle closure attack (< ciliary contraction, less shallowing of angle, compared to any other cholinergic agonist)
- actions slightly different than Ach
- pigment binding
- ocular response - increase accommodation, increase aqueous outflow, others |
|
|
Term
| Ecothiophate (Phospholine) |
|
Definition
36-72 hrs b/c irreversible
Used to diagnose accommodative esotropia
Toxicity - increased vs. pilocarpine or carbachol
Also iris cysts, cataracts, retinal detachment
Indirect Parasympathomimetics
-inhibit AchE – at both muscarinic and nicotinic sites
Long-acting irreversible
Use - glaucoma, accommodative esotropia |
|
|
Term
| Pralidoxime (Protopam, 2-PAM) |
|
Definition
| reactivates AChE undoes ecothiophate/phospholine |
|
|
Term
|
Definition
7-12 days cycloplegia
- last choice - most potent
- contraindications - glaucoma, Down’s syndrome
Antimuscarinics (Anticholinergics, Parasympatholytics)
- direct muscarinic blockers
- cycloplegia
- mydriasis
- decreased ciliary spasm in inflammation
Indications ~ mydriasis
- cycloplegia
- inflammatory disorders in uvea
- myopia
- amblyopia – recent study results |
|
|
Term
|
Definition
| Antidote for atropine/antimuscarinic od |
|
|
Term
| Cyclopentolate (Cyclogyl) |
|
Definition
- 0.5, 1, and 2%
- drug of choice?
- Contraindications
- maximum effect 30-40 min
- duration of maximum action 2-4 hr
- residual effects for 24 hours
- side effects |
|
|
Term
| Tropicamide (Mydriacyl)- 0.5 - 1% |
|
Definition
Antimuscarinic
- maximum mydriasis with one or two drops with in 20-30 min.
- maximum cycloplegia with one drop 2 or 3X at 5 min. intervals
- 20-25 min duration onset; duration 10-40 min
Side effects – rare |
|
|
Term
|
Definition
Antimuscarinic
somewhat M1 selective (theoretically less cycloplegia), currently in clinical trials as a gel (2% twice a day) to treat progressive myopia |
|
|
Term
|
Definition
1% Hydroxyamphetamine and
0.25% Tropicamide |
|
|
Term
|
Definition
1% Phenylephrine and
0.2% Cyclopentolate |
|
|
