Autonomic pharmacology pt. 2 Flashcards Preview

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Flashcards in Autonomic pharmacology pt. 2 Deck (39)
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Where are B1 adrenergic receptors located? What is the effect of stimulation of these receptors?

Heart - stimulation causes increased HR and stroke volume


Where are B2 adrenergic receptors located? What is the effect of stimulation of these receptors?

Lungs - stimulation causes bronchodilation


Where are a1 adrenergic receptors located? What is the effect of stimulation of these receptors?

Blood vessels - effect is vasoconstriction


What does the vagus nerve do to heart rate?

Slows it down


How does serotonin cause migraines?

Constriction of extracranial and intracranial vessels (phase 1)


What does serotonin do to bronchial and GI smooth muscle?



What does serotonin do to skeletal muscle blood vessels and sensory nerve endings?

Dilates skeletal muscle blood vessels and stimulates sensory nerve endings.


What is the main metabolite of serotonin? How is this used clinically?

5-HIAA. 24 hour urine levels can be used to diagnose carcinoid syndrome.


Can serotonin agonists be used prophylactically for migraines? Why or why not?

Nope because these drugs result in constriction of cranial vessels (used during phase 2) and that can precipitate a migraine.


What are the two phases of migraine?

1. Vasoconstriction
2. Vasodilation


___ levels of serotonin in the CNS is associated with depression.



What are ergot alkaloids? What is one clinical use for them? What will too much do?

Serotonin agonists, used sometimes for treatment of migraines. Too much can cause convulsive ergotism and hallucinations.


Name the symptoms of a migraine headache.

Prodroma: Visual disturbances (aura). Then peripheral neuropathy, nausea/vomiting, sonophobia, photophobia.


Can neurotransmitter and/or receptor levels change over time? What is the clinical significance of this?

They do change so patients must be weaned off medications slowly.


Name the headache type that is more common amongst males. What are the symptoms of this type of headache?

Cluster headache. Symptoms include pain on one side of the face, runny nose.


What is melatonin involved in?

Sleep/wake cycles.


Where are a2-adrenergic receptors found? What does stimulation of these receptors do?

They are found on presynaptic neurons in the brain. Stimulation by epi and norepinephrine results in inhibition of release of epi and norepinephrine and subsequent inhibition of adenylate cyclase.


Name the drug that is given to Parkinson's patients because it can cross the blood-brain barrier.



What is Clonidine and what does it do?

It is a sympatholytic that decreases sympathetic neurotransmitter release by stimulating alpha-2 receptors to decrease blood pressure.


What type of receptor do sympatholytics such as Clonidine act on?

Alpha-2 - remember that these receptors result in inhibition of adenylate cyclase and subsequent decrease in NT release.


Parasympathetic activity _______ tear and saliva production.



Is the action of the adrenal gland one reason why the sympathetic division can override the parasympathetic division?



In what cellular location does MAO act? What about cholinesterases?

MAO does its business inside the neuron. Cholinesterases degrade NTs in the cleft.


What is atropine?

An Ach-muscarinic antagonist med that inhibits PNS physiologic responses.


What is the mechanism of action of neuromuscular blockers? What is the difference between a depolarizing and non-depolarizing NMB?

These are Ach receptor antagonists. Depolarizing blockers noncompetitively bind receptors and cause spastic paralysis. Non-depolarizing blockers bind competitively and inhibit muscle contraction (flaccid paralysis).


What are the two methods of action of cholinomimetics?

Directly binding receptors or inhibiting cholinesterase activity.


What is one mechanism by which many antidepressant medications work?

By preventing reuptake by presynaptic catecholaminergic neurons to increase neurotransmitters in the cleft.


Name two sympatholytic drugs and what they do.

Methyl dopa reduces release of norepi to reduce BP. Clonidine is an alpha-2 receptor agonist to reduce epi, norepi and reduce BP.


How can tyramine cause a hypertensive crisis? Where is tyramine found? Which drug amplifies this pathway?

Tyramine displaces norepi from vesicles so lots of norepi is released, increasing BP. Alpha-2 receptors are unable to control norepi release since they are outside vesicles and free to diffuse to the post-synaptic neuron. Tyramine can be found in some aged cheeses, beer, red wine. MAOIs make it way worse.


Should clonidine be given concomitantly with antidepressants?

Nope, they do opposite things!