For the somatic or voluntary nervous system what are the neurotransmitter and receptor involved?
ACH –> Nicotinic M Cholinergic
In the autonomic nervous system, what are the neurotransmitters and receptors?
ACH –> Cholinergic M muscarinic (parasympathetic)
NE –> adrenergic (sympathetic)
What enzyme degrades ACH in the synapse to stop propagation of the nicotinic M cholinergic receptor? What are the two by-products?
ACHesterase. Degrades ACH into acetic acid and choline
Drugs such as physostigmine are used to increase ACH concentration at the neuron synapse, by what mechanism does physostigmine work?
Physostigmine works by blocking ACH esterases. It is an anticholinesterase.
In the parasympathetic system what receptors make up the ganglionic and end receptors? What is the neurotransmitter that activates both?
Ganglionic receptor: Nicotinic N Cholinergic
End Receptor: Muscarinic Cholinergic
ACH is the neurotransmitter
Compare the relative length of the pre- and post-ganglionic fibers in the parasympathetic and sympathetic autonomic nervous systems.
Parasympathetic: long pre-ganglionic, short post-ganglionic
Sympathetic: Short pre-ganglionic and long post-ganglionic
What affect does parasympathetic (muscarinic) activation have on blood vessels?
Some BVs dilate but most only have Sympathetic innervation
When treating xerostomia from Sjogren’s or radiation therapy, one might use a muscarinic agonist such as pilocarpine. What might be some side-affects of pilocarpine? Why?
Increased stomach acid, diarrhea, pillary constriction, bradycardia, & increased sweating. Happens b/c all of these organs also have muscarinic cholinergic receptors, therefore, a parasympathetic reaction will predominate.
Atropine is a muscarinic cholinergic antagonist that might be given to a patient before serious dental surgery to ensure the mouth remains dry. What might be some side affects? What disease should you always check for before prescribing a muscarinic antagonist like atropine?
Tachycardia, pupil dilation (mydriases), constipation, decreased sweating & drowsiness.
Never give atropine to a patient with Glaucoma!
Drugs that block muscarinic cholinergic receptors such as diphenhydramine & scopolamine patches, treat motion sickness due to movement. Why won’t they help with nausea created by opioids or cancer chemotherapy?
B/c motion sickness is activated by muscarinic receptors, while nausea from opioids or chemotherapy is caused by the neurotransmitters Dopamine and Serotonin, which activate different receptors.
What type of drugs are physostigmine and neostigmine? Name a disease/time each one of these drugs might be used. Why is each used for the specific purpose?
Anticholinesterase drugs that inhibit cholinesterases, leading to increased ACH concentration at neuron synapse.
- Physostigmine: Used in the treatment of alzheimers b/c physostigmine has a very high lipid solubility and is therefore able to cross the BBB.
- Neostigmine: Used in the symptomatic treatment of mysthenia gravis, a autoimmune disorder where nicotinic m cholinergic receptors are destroyed. Neostigmine keeps the response from remaining receptors high by keeping the ACH concentrations high at the sites. Charged so doesn’t cross BBB.
Why are nerve gases such as soman, sarin, and toban so dangerous? What acronym describes their affect?
B/c they are extremely lipid soluble, they can enter your body by penetrating skin, and they bind cholinesterases irreversibly.
-SLUDGE Syndrome = Excess Salivation, Lacrimation, Urination, Defecation (Diarrhea), rand mal like seizures, and Emesis (vomiting).
Stimulation of sympathetic alpha-1 receptors results in what? Constriction? Side affect of both?
Stimulation —> Vasoconstriction, can lead to hypertension
Blocking –> Vasodilation, can lead to postural hypotension
What results from Alpha-2 stimulation? Pre-synaptic? Post-synaptic?
Pre-synaptic Alpha-2 receptors decrease neurotransmitter activity. Effectively providing a brake to the system. Provides negative feedback as NE stimulates pre-synaptic alpha-2 receptors.
Post-synaptic alpha-2 receptors have a similar effect to BVs as alpha-1 receptors (=vasoconstriction)
Clonidine is a drug used to decrease BP. How does it work?
Clonidine stimulates pre-synaptic alpha-2 receptors, which decrease norepinephrine release in the synapse leading to less alpha 1 and beta 1 stimulation and lowered BP
What are three ways to lower BP by manipulating sympathetic receptors?
- Block Alpha-1 receptors
- Stimulate Alpha-2 receptors
- Block Beta-1 receptors
What is the main affects of Beta-1 receptors? What Alpha-1 and Beta-1 agonist is often used as a vasoconstrictor w/ local anesthetics?
Increase HR & contractile force. Epinephrine.
What is Propanolol used for? What is its mechanism?
Propanolol is used to lower BP, treat angina and tachychardia. It works by acting as a beta-1 antagonist, slowing HR and decreasing contractile forces.
What happens when Beta-2 receptors are activated?
Dilation. In BVs and Brochioles.
Albuterol (proventil) is used to treat what? Mechanism?
Albuterol is used in the treatment of severe asthma attacks. Albuterol is a Beta-2 adrenergic agonist that results in bronchodilation.
What type of Muscarinic cholinergic drug would be used to treat an asthma attack? Agonist or antagonist?
Muscarinic Cholinergic ANTAGONIST
What is the cause of Parkinson’s disease?
Too much muscarinic cholinergic excitation in the brain (ACH) combined with too little dopaminergic stimulation in CNS (DOP).
What is the problem of treating parkinson’s patients with dopamine?
If dopamine is given in its fully formed state it will not be able to cross the BBB and thus will have no CNS effect. Must be given in the dopamine precursor L-Dopa (amino acid) state.
Isoproterenol was an old anti-asthmatic drug that stimulated Beta-1 & Beta-2 receptors. Why is this combination not ideal for someone having an asthma attack?
B/c stimulating Beta1 receptors increases oxygen demand by increasing HR and contractile forces. This is the last thing you want to do to someone suffering an asthma attack.