This is what I'm doing.

I've gotten a few emails lately about my lack of blogging/emailing. The big question is "What have you been doing?" Well, besides the constraints on my time (class 2 days a week, clinicals 2 days a week, and work 2-3 nights a week) I've been trying to study. Tonight I typed up a "cheat sheet" (that we are allowed to use during a pharm test tomorrow). I thought I would share this with everyone who has been wondering what I've been doing. I miss getting to blog and I promise that as soon as all this school stuff is over, I'll be back to it!! Please excuse the misspellings and craziness of the following. You may not understand it but hopefully, come tomorrow, I will. ha!
Axonal conduction – action potential down the axon (away from the cell body). Synaptic transmission – information carried across the neuron gap. Steps in synaptic transmission – 1.synthesis 2.storage 3.release 4.receptor binding 5. termination. Neurotransmitters of the PNS – acetylcholine (neurotransmitter for muscle), norepinephrine, epinephrine (stimulates every type of PNS receptor), and dopamine. Subtypes of PNS neurotransmitters: Cholinergic receptor – NicotinicN, NicotinicM, and Muscarinic. Adrenergic – Alpha1,2, Beta1,2, and Dopamine. Functions of Adrenergic Receptor Subtypes: Alpha1 (arterioles) vasoconstriction, ejaculation, and contraction of bladder neck and prostate. Beta1 – increases HR, force of contraction, and conduction of AV node, and renin release. Beta2 – bronchial dilation, relaxation of uterine muscle, vasodilation (in very select places), and glycogenolysis. Dopamine – dilates renal blood vessel. Monoamine Oxidase – enzyme that breaks down norepinephrine. MAOI’s inhibit the breakdown of norepinephrine. Muscarinic agonists (rest and digest) used for decreasing urinary retention and increasing GI motility. {Urecholine} Adv.Reac: hypotension, slowed HR, increased salivation, increased gastric acid secretions, abd cramps, diahrrea, exacerb. of asthma, and disrhythmias. Nursing implications: take on empty stomach to prevent gastric upset, record I&O, pee fast, OD (sweating, salivation, incontin, brady, hypotension). {Pilocarpine} used to constrict pupil for tx of glaucoma. Toxicity from muscarinic agonists is treated with atropine. Indirect muscarinic agonists – Acetyl cholinesterase inhibitors: Reversible AChE inhibitors {…mine’s}: used to treat myasthenia gravis, alzheimer’s, to produce constriction in pupils for glaucoma, treatment of anticholinergic poisoning such as OD of antihistamines, tricyclic antidepressants, and phenothiazines. {Prostigmin} Adverse reactions: excessive muscarinic stimulation (sweating, salivating, etc.) and Depolarizing neuromuscular blockade in which muscles contract and relax then stay relaxed (toxic doses could paralyze the resp. muscles; Called cholinergic crisis and treated with atropine). Irreversible AChE inhibitors stay on the receptor until it dies and then it is replaced. Organic insecticide treated with atropine and Valium to control seizures. {Physostigmine} used to treat muscarinic antagonist poisoning. Muscarinic Antagonists (anticholinergics): used pre-op to reduce resp. secretions {Robinol}, mydriasis for eye exam/surg, bradycardia, intst. Cramping and hypermobility {Levsin}, urinary antispasmodic {Urispas}, {Ditropan}, asthma {Atrovent}, muscarinic agonist poisoning {atropine}. Adv. reactions: dry mouth, blurred vision, increased intraocular pressure, urine retention, constipation, decreased sweating, tachy, and complicating asthma by thickening secretions.Neuromuscular blocking agents (nicotinicM antagonists) {..urium’s and succ}: nondepolarizing blocks the receptors without activating them and depolarizing produce muscle contraction, and stay bound preventing repolarization {succinylcholine}. (Will not constrict before relaxing). Will have sore muscles after waking up. Adverse effects: resp. depression, hypotension, brady, card. Arrest, pt. is alert (they just can’t move), and malignant hyperthermia. Adrenergic agonists (fight or flight){epinephrine}: receptors A1&2, B1&2. A1 – vasoconstriction delays absorbtion of local anesthetic, reduces nasal congestion, and elevates BP (in the eye causes mydriasis). B1 – contractility and conductivity in the heart during cardiac arrest. B2 – bronchodilation and drug of choice for anaphylaxis. Adv. Effects: HTN, tachy, dysrhythmias, angina, necrosis at infiltration, hyperglycemia. Norepinephrine {Levophed} – receptor specificity A1, A2, and B1. Isoproterenol (likely to cause dysrhythmias, not often used). Dopamine B1 and high doses A1. Low dose increases HR and contraction. In high doses it could cause the kidneys to work too well which will decrease BP. The higher the dose, the more like norepinephrine. Dobutamine {Dobutrex} B1 : adv. Reactions tachycardia. In CHF causes heart to shrink and work. Works for about 2 weeks. Phenylephrine {Neosynephrine} A1 &2. Nasal spray or IV for vasoconstriction. A2 causes tachyphylaxis (rebound stuffiness). Don’t use more than 3 days. If dependant DC one nostril at a time. {Breathine} B2 used for bronchodilation and uterine hypermotility. To decrease angina caused by giving dopamine, give beta-adrenergic blocker such as porpranolol. Alpha-2 agonists decrease BP by tricking the body into thinking there is too much epinephrine. Used to treat HTN. Clonidine {Catapres}. Adv. Effects are sedation, ortho hypotension. Adrenergic Antagonists: Alpha receptor bloackers terazocin {Hytrin}. Used for HTN, BPH (helps to start urine stream), pheochromocytoma, and Raynaud’s because they vasodilate. Adv. Effects ortho Hypotension (1st dose syncope, give at HS, and start low and go slow), reflex tachy, nasal congestion, and impotence. Beta receptor blockers – {propanolol, metoprolol, and atenolol} – reduce HR, force of contraction, reduced conduction, suppression of renin release and decrease BP and HR. Used for HTN, angina, dysrhythmias, MI (give beta blocker and they live longer), heart failure (decreased cardiac output), hyperthyroidism, migraine (prevention not tx), stage fright, pheochromocytoma (give alpha and beta blocker), and glaucoma (make pupils smaller). Adv. Effects: sedation, brady, AV block, decreased cardiac output, bronchoconstriction (with atenolol and metoprolol), inhibition of glycogenolysis, and delay awareness of hypoglycemia. Nicotinic receptors are located in PNS and SNS. 3 receptors activated by aceylcholine and their location: nicoinicM – postsynaptic fibers in the PSNS and SNS. nicotinicN – skeletal muscle. Muscarinic – end receptors of the PSNS. Two neurotransmitters that act only on the SNS: epi and norepi. Sympathetic stimulation of adrenal medulla leads to secretion of epi. Synonym: Sympathomimetic – adrenergic, adrenergic agonist. Sympatholytic – adrenergic antagonist, adrenergic blocker. Parasympathomimetic – cholinergic, muscarinic. Parasympatholytic – anticholinergic, muscarinic antagonist, cholinergic blocker. Stimulation of which receptor will cause the following? Alpha1: pupil dilation, bladder neck constriction, and increased BP. Beta1: increased HR and BP. Beta2: bronchiolar dilation and dilation of arterioles of the heart. Muscarinic: pupil constriction, bladder emptying, and peripheral vasodilation. Nicotinic: contraction of skeletal muscle. Antagonism (blocking) of these receptors will produce? Alpha1: papillary constriction, bladder emptying, dilation of the arterioles of the skin. Alpha2: increased BP. Beta1: decreased HR. Beta2: uterine contraction. Muscarinic: pupillary dilation, increased HR, bronchiolar dilation, urinary retention, decreased lung secretions, constipation. Drugs and the effects they produce: Alpha1 agonist: papillary dilation, increased BP. Alpha1 blocker: papillary constriction, impotence. Beta1 agonist: increased HR and BP. Beta1 blocker: decreased HR and BP. Beta2 agonist: bronchiolar dilation and uterine relaxation. Beta2 blocker: bronchiolar constriction and uterine contraction. Cholinergic agonist: pupillary constriction, decreased HR, bronchiolar constriction, increased peristalsis, & increased bladder tone. Anticholinergic: pupillary dilation, increased HR, bronchiolar dilation, decreased peristalsis, relaxation of bladder spasms, and impotence. Chemical responsible for the breakdown of norepi? Monoamine Oxidase. A chemical that blocks the action of acetylcholinesterase will effect: pupil constriction, salivation, and increase intestinal motility. Neuropharmacology drugs act by altering synaptic transmission.
*Post-ganglionic neuron of the SNS is the adrenal medulla. *Activation of beta1 receptors causes increased HR and force of contraction. *The action of indirect-acting parasympathomimetics is to inhibit or inactivate the enzyme aceylcholinesterase, thus permitting the accumulation of acetylcholine at the receptors. *Narcotic analgesics are safe to administer with atropine. *If a pt develops muscarinic antagonist toxicity from ingestion of a chemical, administer physostigmine. *Pancuronium does not depress the CNS. * When tubocurarine is administered, will see paralysis in levator muscle of eyelid and muscles of mastication. *Difference between succ and the nondepolarizing neuromusclular blockers: paralysis is preceded by a brief initial period of contraction. * Directi mechanism by which adrenergic agonists activate adrenergic receptors: direct receptor binding. *A patient with heart failure would benefit from a beta1 agonist. *Etiology for expected orthostatic BP change with an Alpha1 blocker: dilation of peripheral arterioles. *A pt with asthma who requires a beta-blocker should be treated with metoprolol. *GI upset is common with beta blockers. Symptoms of “anticholinergic side effects” are dry mouth, constipation, urinary retention, bowel obstruction, dilated pupils, blurred vision, increased HR, and decreased sweating. Also causes impairment in cognitive functioning.
Post note: Yes, I was able to fit all of this on one 8.5X10 sheet of paper!