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OU PDA > Exam 1 II Objectives > Flashcards

Exam 1 II Objectives Flashcards

1
Q

Properties of ANS

A
  • all output from CNS to body except motor / skeletal muscle
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2
Q

List the processes which the ANS controls

A
  • Heart function
  • Visceral organ function
  • Breathing
  • Digestion
  • Blood flow to organs
  • Contraction / relaxation of smooth muscle
  • Exocrine and endocrine hormones
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3
Q

Preganglionic pathways

A
  • ACh synapse on nicotinic receptors which releases NT to synapse on post-ganglionic receptors
  • Every preganglionic neuron is releasing ACh
  • ACh that synapse on nicotinic receptors in adrenal medulla causes it to release Epi and NE
  • ACh can directly synapse on nicotinic receptors on skeletal muscle
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4
Q

Prostganglionic pathways

A
  • ACh (from nicotinic) synapse on muscarinic receptors on cardiac & smooth muscle, gland & sweat cells, and nerve terminals
  • NE (from nicotinic) synapse on alpha and beta receptors on cardiac & smooth muscle, gland cells, and nerve terminals
  • Dopamine (from nicotinic) synapse on D1 receptors on vascular smooth muscle
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5
Q

Neurotransmission mechanism

A

Ion channels open at nerve terminal -> Ca influx trigger vesical to release content via fusion of SNAPS and VAMPS

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6
Q

What muscle is located in the iris?

A

Pupillary dilator and constrictor muscle

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7
Q

Which muscle is responsible for mydriasis?

A
  • mydriasis: pupil dilation

- contraction of radial pupillary dilatory muscle

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8
Q

What does β adrenoceptor activation do to the eye?

A
  • Increase secretion of aqueous humor from the ciliary epithelium
  • Increases intraocular pressure
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9
Q

Mechanism for glaucoma

A
  • inability to drain fluid
  • increase in intraocular pressure
  • damaged optic nerve
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10
Q

Identify the neurotransmitter acetyl choline and the steps involved in its synthesis, storage, release and termination of acetylcholine.

A
  • Choline transporter (CHT) cotransports choline and Na into the nerve terminal
  • AcCoA + Choline -> ACh
  • VAT transports this into storage vesicle
  • Increase in intracellular Ca2+ causes VAMPs and SNAPs to merge -> release of ACh
  • AChesterase breaks down ACh into acetate and choline
  • Choline transported into nerve terminal
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11
Q

List the drugs that target each of these steps as a mechanism of neuromodulation.

A
  • Hemicholinium blocks CHT
  • Vesamicol blocks VAT
  • Botulinum toxin blocks release of ACh from vesicles
  • Latratoxin and Carbachol increases release of ACh
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12
Q

M2 receptor tissue distribution

A
  • myocardium
  • smooth muscle
  • CNS neurons
  • “some presynp. sites”
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13
Q

M3 receptor tissue distribution

A
  • exocrine glands
  • vessels
  • CNS neurons
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14
Q

M2 mechanism

A
  • opening of K channels

- inhibition of adenylyl cyclase

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15
Q

M3 mechanism

A
  • formation of IP3 and DAG

- increased intracel. Ca

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16
Q

Acetyl Choline as a Cholinomimetics

A
  • Low doses = only M receptors
  • High doses = both M and N receptors
  • Used to produce miosis during ophthalmic surgery
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17
Q

Bethanechol as a Cholinomimetics

A
  • Only choline ester with common clinical use
  • Used for: post-operative therapy, esophageal reflux
  • Resistant to inactivation by AChE
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18
Q

Methacholine as a Cholinomimetics

A
  • Partially resistant to AChE inactivation

- In the past, used for diagnostic tool for asthmatics

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19
Q

Carbachol as a Cholinomimetics

A
  • Resistant to AChE inactivation
  • Bind and activate M receptors
  • Releases ACh from nerve endings
  • Used to produce miosis in patients with glaucoma
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20
Q

Nicotine as a Cholinomimetics

A
  • Activates ALL nicotinic receptors

- If given at high doses, it will block nicotinic receptors

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21
Q

Muscarine as a Cholinomimetics

A

Activates all muscarinic receptors

- Atropine is the antidote for this

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22
Q

Pilocarpine as a Cholinomimetics

A
  • Stimulates muscarinic receptors
  • Can cross BBB
  • Used to treat glaucoma
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23
Q

Reversible AChE inhibitor agents property

A

allow the regeneration of AChE within hours

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24
Q

Physostigmine

A
  • reversible AChE inhibitor
  • Binds to both sites on AChE
  • Can cross BBB
  • Used for glaucoma; increase amounts of ACh -> miosis
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25
Q

Neostigmine

A
  • reversible AChE inhibitor
  • Cannot cross BBB
  • Directly stimulate nicotinic sites on skeletal muscle
  • Used for Myasthenia Gravis (MG)
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26
Q

Pyridostigmine

A
  • reversible AChE inhibitor
  • Used for MG
  • Potent AChE inhibitor
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27
Q

Ambenonium

A
  • reversible AChE inhibitor
  • Used for MG
  • Potent AChE inhibitor
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28
Q

Edrophonium

A
  • reversible AChE inhibitor
  • Bind only to anionic site
  • Short acting / short duration of action
  • Used to diagnose MG
  • Helps with titration of longer acting anticholinesterase
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29
Q

antidote to curare poisoning

A

All reversible AChE inhibitors are antidotes

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30
Q

Which drugs are used to attempt to treat cognitive dysfunction?

A
  • Tacrine
  • Donepezil
  • Rivastigmine
  • Galantamine
  • These are reversible AChE inhibitors
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31
Q

Irreversible AChE inhibitor agents property

A
  • Contains phosphorous -> phosphorylate esteratic site on AChE (covalent bond)
  • lipid soluble; absorbed through skin
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32
Q

Echothiophate

A
  • irreversible AChE inhibitor
  • Potent miotic
  • used for glaucoma
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33
Q

Parathion

A
  • irreversible AChE inhibitor
  • Insecticides / pesticides
  • Converts to paraxon in liver
  • Potent AChE inhibitor
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34
Q

Malathion

A
  • irreversible AChE inhibitor
  • Insecticides / pesticides
  • Converts to malaoxon in liver
  • Potent AChE inhibitor
  • Quickly inactivated in mammals and birds
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35
Q

What is the name for the potent war gases?

A
  • Sarin
  • Soman
  • Tabun
  • cannot be reversed UNLESS given RIGHT AFTER exposure
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36
Q

List one drug available for treatment of toxicity from overdose of anticholinesterase inhibitors and its mechanism of action.

A

Pralidoxime (2-PAM): releases the organophosphate from the esterase

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37
Q

Explain why ACh itself is not a good drug

A
  • Non-selective
  • Fast hydrolysis
  • Poor bioavailability
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38
Q

Explain the studies to understand the impact to “stereochemistry of Ach”

A
  • Wanted to know which conformer was physiologically active
  • Hypothesized that anti-periplanar was because it has less steric hindrance
  • Found that the anticlinal form had stronger affinity
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39
Q

Methacholine structure

A
  • introduction of methyl group reduce activity

- Higher affinity for mACh than nACh

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40
Q

Carbachol structure

A

Have carbomyl group -> less electrophilic carbonyl carbon -> tolerant to / slows down hydrolysis

41
Q

Explain why norepinephrine itself is not a good drug

A
  • Non-selective
  • Poor oral bioavailability
  • Undergoes fast metabolism
    • MAO & COMT in intestine and liver (1-2 min duration of action)
    • 3’-O-glucuronidation / sulfation
42
Q

Anti-muscarinic mechanism

A
  • Interfere with synapse on muscarinic receptors (receives innervation from Nn)
  • Muscarinic receptors present on/in: cardiac & smooth muscle, gland cells, sweat glands, nerve terminals
43
Q

Ganglion blockers mechanism

A

Interfere with synapse on nicotinic neuronal receptors

44
Q

Neuromuscular blocking agents mechanism

A
  • Interferes with synapse on Nm

- Inhibited irreversibly by snake alpha-bungarotoxins

45
Q

Atropine

A
  • anti-muscarinic
  • Cross BBB; CNS stimulant
  • Effects on eye: mydriasis (dilation), cycloplegia (where eye cannot focus)
  • Decreased GI & urinary motility
  • Low dose -> bradycardia
  • High dose -> tachycardia
  • Toxic dose -> vasodilation
  • Clinically used for: anti-spasm, anti-secretory (for dentists), antidote for cholinomimetic poisoning
  • Can lead to: dry eyes, xerostomia, hyperthermia, hallucinations, delirium, coma
46
Q

Scopolamine

A
  • anti-muscarinic
  • Cannot cross BBB; CNS depressant
  • Prevent motion sickness
  • Can produce euphoria
47
Q

Tropicamide and Cyclopentolate

A
  • anti-muscarinic

- Less potent; useful for ophthalmic exams

48
Q

Ipratropium

A
  • anti-cholinergic
  • Does not cross BBB
  • Treat COPD, bronchitis, and emphysema
  • dose QID
49
Q

Tiotropium

A
  • anti-cholinergic
  • Does not cross BBB
  • Treat COPD, bronchitis, and emphysema
  • dose QD
50
Q

Benztropine and trihexyphenidyl

A
  • anti-muscarinic
  • CNS acting agents
  • Used for Parkinson’s patients
51
Q

Nicotine

A
  • ganglion blocker
  • Low dose = stimulate Nn receptors; used for tobacco cessation
  • High dose = blocks ganglia
  • Acute overdose leads to: CV & CNS stimulation, increased GI activity, N/V, abdominal pain, dizziness, confusion, muscle weakness
52
Q

Hexamethonium

A

ganglion blocker

53
Q

Varenicline (Chantix®)

A
  • nicotinic agonist
  • Smoking cessation
  • Side effects: headache, nausea, insomnia
54
Q

Competitive Nondepolarizing neuromuscular blocking drugs

A
  • Low doses = compete with ACh to bind to the Nm receptor to prevent depol
  • High doses = block ion channels in the endplate -> cannot undergo neuromuscular transmission -> paralysis of muscle
55
Q

D-Tubocurarine (curare)

A
  • neuromuscular blocking agents
  • Also blocks autonomic ganglia -> hypotension
  • Releases histamine from mast cells -> bronchoconstriction
56
Q

Doxacurium

A
  • neuromuscular blocking agents
  • Doesn’t block ANS ganglia, doesn’t release histamine
  • If cannot clear due to renal failure -> prolonged muscle relaxation
57
Q

Pancuronium

A
  • neuromuscular blocking agents
  • has a steroid nucleus
  • Doesn’t block ANS ganglia, doesn’t release histamine
  • If cannot clear due to renal failure -> prolonged muscle relaxation
58
Q

Atracurium

A
  • neuromuscular blocking agents
  • Intermediate acting
  • Release histamine from mast cells
  • Metabolite can provoke seizures
  • Preferably given to asthmatic patients
59
Q

Cistacurium

A
  • neuromuscular blocking agents

- Isomer of atracurium but does not have seizure side effects

60
Q

Vecuronium & Rocuronium

A
  • neuromuscular blocking agents

- Doesn’t block ANS ganglia nor release of histamine

61
Q

Mivacurium

A
  • neuromuscular blocking agents
  • Shortest acting
  • Mainly used in surgery
62
Q

Succinylcholine

A
  • neuromuscular blocking agents
  • Short acting depol blocks muscle for 5 minutes
  • Releases histamine
  • Stimulates autonomic ganglia -> elevation of blood pressure
  • Increase CSF & GI pressure
  • Contraindicated in glaucoma patients, patients with brain tumors, immediately after a meal
  • Drug of choice to relax laryngeal muscles prior to intubation
  • Adverse effects: bradycardia, fasciculations, muscle pain, hyperkalemia, increase IOP, hyperthermia
63
Q

EPI

A
  • Immediate relief from hypersensitivity reactions (anaphylactic shock)
  • Adjuvant with anesthesia and topical hemostatic agent due to its vasoconstrictor effect
64
Q

DA

A
  • used in CHF patients; an adjuvant to reduce periph. Resistance
  • infusion has been used to treat certain conditions where renal blood flow is compromised
65
Q

Isoproterenol (ISO)

A
  • Nonselective β-adrenoceptor agonist
  • relieve bronchoconstrictive episodes in asthmatic patients and COPD
  • Sometimes used in emergencies to stimulate heart rate in patients with bradycardia or heart block.
66
Q

Ephedrine

A
  • Nonselective β-adrenoceptor agonist
  • used orally for bronchial asthma (β effect)
  • decongestion
  • used for its α effects as a pressor agent -> produce short lasting mydriasis without cycloplegia
67
Q

Pseudoephedrine

A
  • Nonselective β-adrenoceptor agonist
  • Decongestant
  • Must not be taken in patients with HTN risk
68
Q

Dobutamine

A
  • Selective β2-adrenoceptor agonists
69
Q

Metaproterenol

A
  • Selective β2-adrenoceptor agonists

- used primarily to treat bronchial asthma

70
Q

Terbutaline

A
  • Short-acting β2-adrenoceptor agonists
71
Q

Albuterol

A
  • Short-acting β2-adrenoceptor agonists
  • Treatment of asthma
  • Long acting; fewer cardiac side effects
72
Q

Ritodrine

A
  • Selective β2-adrenoceptor agonists
  • β2-adrenoceptor agonist
  • some cardiac effects possible
  • approved to relax smooth muscle of the uterus to delay premature labor
73
Q

Phenylephrine

A
  • Selective α1-adrenoceptor agonist

- α-adrenergic stimulants -> local vasoconstriction in nose -> less leakage of fluid

74
Q

Methoxamine

A
  • Selective α1-adrenoceptor agonist
  • used to produce mydriasis
  • treat paroxysmal atrial tachycardia
75
Q

Clonidine

A
  • Selective α2-adrenoceptor agonist
  • Crosses BBB
  • Decrease sympathetic tone to the blood vessels and heart
  • Treat excessive sympathetic activity experienced during withdrawal from opioid and ethanol addiction (gives synergy effect with opioid  opioid dose can be decreased)
76
Q

α-Methyl Dopa

A
  • Selective α2-adrenoceptor agonist
  • Crosses BBB
  • Metabolite is potent α2-agonist
  • Decreased sympathetic tone
  • Not metabolized by MAO -> longer CNS effect than NE
77
Q

Tyramine

A
  • ## causes a massive release of NE from sympathetic nerve endings
78
Q

Amphetamine and Methamphetamine

A
  • Produce temporary increased mood but decreased appetite
  • Patients suffering from narcolepsy.
  • Some hyperkinetic children respond to amphetamines more sedated and thus ↑ their attention span.
79
Q

Methylphenidate (Ritalin)

A
  • CNS stimulant large doses = CNS excitations, can cause convulsions
  • Used in children with ADHD
80
Q

Tricyclic antidepressants

A

potent inhibitors of catecholamine reuptake into adrenergic nerve terminals

81
Q

Drug-drug interaciton between sympathomimetics and MAO inhibitors

A

Pre-treatment with cocaine or TCA -> Inhibits effects of Tyramine, amphetamine, guanethidine and 6-hydroxy Dopamine

82
Q

αadrenoceptor antagonists

A
  • α-Adrenoceptor antagonists prevent sympathetic tone to the blood vessels.
  • Sympathetic innervation to the heart is functional (β1 receptor-mediated).
  • Side effects: orthostatic htn, reflex tachycardia, nasal congestion, failure to ejaculate
83
Q

β-adrenoceptor antagonists

A
  • Antagonism of the innervated β1-adrenoceptors
  • Eliminate sympathetic neural effectiveness to heart and JDA in kidney (which decreases renin release)
  • Consequences: bronchoconstriction, vasoconstriction, lipolysis, glycogenolysis
84
Q

Recognize and list the clinical uses of all drugs targeting the adrenergic system

A
  • Hypertension
  • Essential tremor
  • Glaucoma
  • Post-infarction prophylaxis
  • Angina
  • Congestive heart failure
  • Migraine
  • Stage fright
  • Cardiac arrhythmias
  • Pheochromocytoma
  • Autonomic hyper-reflexia
  • Raynaud’s
  • Benign prostatic hypertrophy
  • Hyperthyroidism
85
Q

Phentolamine

A
  • α-adrenoceptor Antagonists
  • antagonist that competes with NE on the α- adrenoceptors
  • selective: a1 > a2
  • short duration of action due to competition with NE
86
Q

Phenoxybenzamine

A
  • α-adrenoceptor Antagonists
  • Potent
  • Higher affinity for a1 than phentolamine
  • Long duration of action b/d dual mechanism of blockade; first starts as competitive antagonist -> after 30-60 minutes it becomes non-competitive
87
Q

Prazosin

A

tension -> some people lose consciousness with first administration

88
Q

Terazosin and Doxazosin

A
  • α-adrenoceptor Antagonists
  • Prazosin-like drugs with a longer half-life which permits once daily dosing
  • Commonly used to treat the symptoms of benign prostatic hypertrophy/hyperplasia (BPH).
89
Q

Yohimbine

A
  • α-adrenoceptor Antagonists
  • Selective for a2
  • Experimental tool; prevents hypotensive effects in clonidine and α-methyldopa
90
Q

Propranolol

A
  • β-adrenoceptor Antagonists
  • Blocks both beta1 and beta2
  • Potent local anesthetic
91
Q

Metoprolol

A
  • β-adrenoceptor Antagonists
  • High affinity beta1 > beta2 and therefore called cardioselective
  • Decreases plasma renin levels
  • Less affinity to beta 2  less metabolic and bronchial effects
  • Side effects: fatigue, dizziness, headache, insomnia
92
Q

Atenolol

A
  • β-adrenoceptor Antagonists
  • Cardioselective
  • Longer half life
  • Less side effects than metoprolol
  • Excreted by kidney and therefore should not be given to patients with renal failure / disease
93
Q

Esmolol

A
  • β-adrenoceptor Antagonists
  • Cardioselective
  • Short half-life when given IV b/c of RBD esterases
  • Used for acute emergency control of ventricular heart rate in patients with atrial fibrillation or atrial flutter
  • Safer to use in critically ill patients
94
Q

Betaxolol

A
  • β-adrenoceptor Antagonists
  • Cardioselective
  • Long half-life; once daily administration
95
Q

Pindolol

A
  • β-adrenoceptor Antagonists
  • Has ‘intrinsic sympathomimetic’ activity
    • Non selective beta antagonist but stimulates beta1 as well
  • Less cardiac depression than other drugs
  • Better tolerated during exercise
96
Q

Timolol

A
  • β-adrenoceptor Antagonists
  • Potent; non-selective
  • Reduces formation of aq. humor in eye; less side effects than other drugs
  • Open angle glaucoma
97
Q

Nadolol

A
  • β-adrenoceptor Antagonists
  • Long half life; once daily administration
  • Not selective
98
Q

Labetalol

A
  • α and β-adrenoceptor Antagonists
  • nonselective β-AR antagonist & α1 selective blocker
  • Higher potency for beta but alpha dominates because they are located on the blood vessels
  • some β2 stimulating properties
  • post. hypotension is a problem in some patients
  • decrease TPR with little effect on HR and CO
99
Q

Carvedilol

A
  • α and β-adrenoceptor Antagonists
  • nonselective β-AR antagonist & α1 selective blocker
  • Has “free radical scavenger” antioxidant properties
    • can bind to and scavenge reactive oxygen species
    • decrease biosynthesis of ROS and oxygen radicals
  • Very lipophilic -> protects cell membranes from lipid peroxidation
  • Prevents LDL oxidation

OU PDA (8 decks)

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