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Flashcards in CIS Fitz Deck (13):

66 y/o F surgery. General anesthesia: sufentanil and propofol. Cisatracurium for tracheal intubation. Ephedrine to treat decrease in arterial blood pressure.
Pupil diameter monitoring during procedure showed miosis. Which drug caused this?

Mu agonist
Clinical effects: euphoria, CNS and resp depression, drug dependence, *MIOSIS*, GI & uterine motility


How does acetazolamide lower intraocular pressure?
A. Remodels uveoscleral pathway
B. Increases lumen of Schlemm's canal
C. Binds to prostanoid receptors
D. Contracts ciliary muscle
E. Inhibits aqueous humor secretion

E. Inhibits aqueous humor secretion
Carbonic anhydrase inhibitors directly target catalytic formation of bicarbonate (HCO3-), which is the driving force for aqueous humor secretion.

Topically effective inhibitors need to inhibit >99% of enzymes
Dorzolamide and brinzolamide
Only intermediate efficacy


How does apraclonidine lower intra-ocular pressure?
A. Antagonism of alpha1 adrenergic receptors
B. Antagonism of beta1 adrenergic receptors
C. Agonist of muscarinic cholinergic receptors
D. Agonist of prostanoid receptors
E. Agonist of alpha2 adrenergic receptors

E. Agonist of alpha2 adrenergic receptor (pre-synaptic)
Lessens aqueous humor secretion from ciliary epithelium


How do timolol and betaxolol lower intraocular pressure?

Beta adrenergic receptor antagonists

Betaxolol = Beta1 selective (cardioselective=less risk in asthmatics)

Lessens aqueous humor secretion from ciliary epithelium


Describe effects of epinephrine in eye

Epi at alpha1 adrenergic receptors on radial smooth muscle->contraction->mydriasis

Epi at beta2 adrenergic receptors->relaxation of ciliary muscle


Describe iris sphincter muscle innervation

Innervated by cholinergic fibers to muscarinic M3 receptors

Agonists at M3 receptors (acetylcholine, carbachol, pilocarpine) cause pupil constriction (miosis)

Antagonists of cholinergic tone at M3 receptors (cyclopentolate, atropine, scopolamine) cause pupil dilation (mydriasis)


Describe radial muscle innervation

Innervated by adrenergic fibers to alpha1 receptors

Agonists at alpha1 receptors (phenylephrine, dipivefrin, epinephrine) cause pupil dilation (mydriasis)


Describe the parasympathetic and sympathetic pathway to the eye for constriction/dilation

Oculomotor nerve->ciliary ganglion->Ach->Sphincter muscle (M3 muscarinic)

Superior cervical ganglion->NE->Radial muscle (alpha1 adrenergic)


35 y/o F history of migraine since 22. Daily headaches for 1 yr. 6-8 Vicodin 7.5mg/day and Zomig 5-10mg/day. Topirimate, propranolol, escitalopram (selective serotonin reuptake inhibitor SSRI) were not helpful. Fibromyalgia, so Cymbalta (Duloxetine=Serotonin/NE reuptake inhibitor) 30 mg/day.
1. Diagnosis?
2. She was given dihyrodergotamine (DHE) IV to prevent withdrawal headache. She was treated with ondansetron (serotonin 5HT3 antagonist) IV prior to DHE. Why?
3. Ketorolac IV was given for breakthrough headache. Clonidine in patch was given to prevent withdrawal symptoms. What other types of pain relief would you consider?

1. Chronic migraine with medication overuse headache
2. Prevent nausea and vomiting
3. Non-narcotic analgesic like acetaminophen, NSAIDs. Ketorolac is only NSAID in injectable form.
Others; diclofenac, diflunisal, etodolac, fenoprofen, fluriprofen, indomethacin, mefenamic acid, nabumetone, oxaprozin, piroxicam, sulindac, tolmetin


Clonicdine is related structurally and pharmacologically to apraclonidine. What is the mech of action of apraclonidine?
A. F prostanoid agonist
B. Adrenergic Beta1/2 receptor antagonist
C. Adrenergic alpha2 receptor agonist
D. Cholinergic muscarinic receptor agonist
E. Acetylcholinesterase inhibitor

C. Adrenergic alpha2 receptor agonist


Newborn M. Difficulty breastfeeding, lethargy at day 7. At day 11, concerns of skin color and lethargy. Day 13, baby cyanotic without vital signs. Resuscitation unsuccessful. Full postmortem analysis showed no anatomic cause of death. Mother was prescribed Tylenol3 (codeine and acetaminophen) to relieve pain from episiotomy.
1. Was codeine too potent an analgesic?
2. Developmental or genetic factors involved?
3. How to prevent this tragedy?

1. No, it is a weak mu agonist. However, some analgesic effect of codeine derives from its metabolic conversion to morphine by liver
-Codeine (methoxymorphine) -> O-dealkylation CYP2D6 -> morphine

2. Maternal CYP2D6 polymorphisms govern rate of morphine delivery to breast-fed neonate. Fast = more morphine
-Neonatal renal and hepatic clearance processes are developmentally immature. Clearance in neonate->slow->few UGT metabolites in urine

3. Prescribe codeine for only 2-3 days to nursing mothers. Genotype (rarely done). Non-narcotic analgesic. Maintain high index of suspicion


Describe morphine metabolism and renal clearance

->UGT->M3G (active)
->UGT->M6G (active)
->CYP-> Nor-m (inactive)
->dehydrogenase->hydromorphone (active)


Previously healthy 2 y/o M found with 1 tablet of suboxone (8 mg buprenorphine/2 mg naloxone) in his mouth. Remnants of partially dissolved table was removed. Child experienced 1 episode of spontaneous emesis and became drowsy on way to ED 30 min after exposure. Pt was observed. No interventions necessary, and child discharged asymptomatic and stable 6 hrs after ingestion.
What contributed to the favorable outcome?
A. Buprenorphine is a partial agonist at mu opioid receptors
B. Naloxone in tablet limited response to buprenorphine
C. Hepatic metabolic capacity in infant is fully mature
D. Respiratory rate in a 2 y/o is greater than in adult

B. Naloxone in table limited response to buprenorphine
Naloxone competitively inhibits mu agonists