My life has been a little crazy lately. Most everyone knows that. This week has definitely started off with a bang!
I'll start at the beginning (from my point of view of coarse)! My oldest daughter was grounded last week. We won't get into the reasons. Let's just say that she didn't exactly have to stay after school to run for cross country. This morning (the one day that class starts late for me and I don't have to work so I sometimes get to sleep in until the house is empty) I was rudely awaken by banging on my bedroom door. I peeled open my groggy eyes, croaked out "come in", waiting a few seconds, cleared my throat, and yelled "COME IN". Still now response. I stumbled out of bed, tripped over a pillow in the floor, fell into the door and then managed to right myself as I yanked open the door. There, standing in the hall, was my teenage daughter. Her big brown eyes, bright with tears. She starts immediately with "Daddy won't let me go to (nearby town) with band. I have to go, it's extra credit!" Well, we proceed to tell her that extra credit is an unnecessary activity that she was grounded from last week. She manages to have a teenage-girl fit. I tell her to go wait on the bus. She stands in the garage until the bus gets here. When it comes, she doesn't get on it! I end up taking her to school with my (uncombed, curled, straightened, or otherwise fixed) hair in a clip, puffy eyes, and snoopy P.J.'s. I dropped her right at the front door without saying a word. I kept thinking, "Oh, yea. We'll see how you feel when your friends see just how bad your mom looks in the morning." That was, until I realized that her friends paid no attention to me. It was the parents that were looking at me like I had just rolled outta bed or something. Dog-gone em!
So, I went to class. I drive about 40 miles through woods, with no cell signal (not that it would matter because I forgot my phone at home today) to get to school by the way. I went to my first class (which I have a test in tomorrow) and decided that I should probably just skip pharmacology to go home and study. I made it about half way home when I heard the most awful racket coming from my little red car. It wasn't shaking or shivering so I didn't think that it was a flat tire but I pulled over to check it out. Oh yes, it was flat. I managed to get help from a little guy who looked just like the wrecker driver from Adventures in Babysitting. No, I am not kidding. He had the big scruffy beard, no teeth, and a railroad engineer hat with the bill flipped up. The only discernible difference was that he had two hands and no hook. He was wearing a six-shooter on his right hip though. We managed to get the little spare on my car only to see, after we lowered it, that it was half-flat as well! He tells me that he has an air compressor at his house across the highway. I really had no choice. It was either to drive across there for air or risk making a crazy looking little man, wearing a gun on his hip, mad at me. At this point I was almost sick. He really was a nice guy in the end. While his compressor filled up, he chit-chatted about his life. He offered me a cold beer. I refused. Although, I did tell my sister later that if I hadn't been driving, I might have taken him up on his offer. So, I finally got home.
My husband asked about my day. He said that he promised that his bad day could out-do my bad day. Come to find out, while I was out of commission, my husband got a call from the high school principle. My oldest son was suspended from school. FOR FIGHTING!!! I called my mom to get some much needed advice. Do you know what she told me? I'm not supposed to be their friend! Seriously. Who would have thought it? I'm supposed to be the parent? Just kidding. I know that. I have tried to hard to make my kids like me. It's jacked up, I know.
So, I'm sitting here writing this blog and I get a call from GG (father-in-law) to inform me that my youngest son's teacher has sent him an email because she doesn't have either mine or my husbands. My youngest son has a small, well big problem with organization and staying on track. (I wonder where he got that from?) He forgot his book at school that he is being tested over tomorrow. Luckily it worked out that we were able to get into the school to get his book. So, our house is pretty much on lock-down. I have not studied at all for my test. (Why are you blogging, you ask? Because it's therapeutic. Leave me alone!)
I haven't prayed for patience. I did tell my husband yesterday that I was almost at my breaking point with everything going on right now. Ha! I've heard people say that God has a funny sense of humor. I guess I wasn't that close to breaking after all!
Monday, September 29, 2008
Monday, September 22, 2008
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!
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!
Tuesday, September 9, 2008
How Time Flies
Fall is always a special time for me. I used to hate it. It was cold and I knew it wouldn't be long before melancholy set in. That was until I met my man. I think that is so funny. It's amazingly easy to write "my man" but I've tried to say it out loud. Nope, doesn't sound right. Anyway...
After talking to my sister (who I miss very much) on the phone tonight, I realized that nine years ago last night was a very special night.
My sister and I had been riding horses that day. We were having a great time until her horse got spooked and bolted. Unfortunately her boot got stuck in the stirrup. As she was being drug, the horse was also stomping her. Long-story-short, she ended up in an ambulance. In the commotion, the horses were turned loose. When word got out about Mandee, someone got the word to Shawn, who was friends with my parents and it was a friend of a friend kind of thing. Shawn helped me catch the other horse and unsaddle them. He then gave me a ride to the hospital to check on my sister.
At the time, we hadn't spent much time together at all. He was all about finishing his thesis. I was all about hating men. BUT, there was still an attraction there.
Shawn waited in the ER waiting room with me for a couple of hours until they said that Mandee was going to be okay. Shawn and I walked outside while Mandee was being discharged. The sun was behind the hill and the wind was just starting to get chilly. Standing there chatting about nothing important, Shawn ask me about places that I had lived. In my bitterness I said, "I'll never leave Fayetteville again!" There was a long pause and I looked up at Shawn's face. He had the strangest grin on his face. We ended up leaving that night without saying too much more. We were engaged on Valentines day.
(Picture taken not long after becoming engaged. I look like I'm correcting his posture.)Then we were married in May and moved to Little Rock the next weekend. Not long after we were married, Shawn and I were talking about the first time we ever really talked to each other. I told him about the weird grin on his face when I told him that I would never leave Fayetteville again. He laughed and said, "I was right." Puzzled, I asked what he was talking about. He said, "When you said that, the first thought that went through my head was that when you marry me you will!"
So, nine years and still not in Fayetteville. That's okay. The trade-off has been worth it!
After talking to my sister (who I miss very much) on the phone tonight, I realized that nine years ago last night was a very special night.
My sister and I had been riding horses that day. We were having a great time until her horse got spooked and bolted. Unfortunately her boot got stuck in the stirrup. As she was being drug, the horse was also stomping her. Long-story-short, she ended up in an ambulance. In the commotion, the horses were turned loose. When word got out about Mandee, someone got the word to Shawn, who was friends with my parents and it was a friend of a friend kind of thing. Shawn helped me catch the other horse and unsaddle them. He then gave me a ride to the hospital to check on my sister.
At the time, we hadn't spent much time together at all. He was all about finishing his thesis. I was all about hating men. BUT, there was still an attraction there.
Shawn waited in the ER waiting room with me for a couple of hours until they said that Mandee was going to be okay. Shawn and I walked outside while Mandee was being discharged. The sun was behind the hill and the wind was just starting to get chilly. Standing there chatting about nothing important, Shawn ask me about places that I had lived. In my bitterness I said, "I'll never leave Fayetteville again!" There was a long pause and I looked up at Shawn's face. He had the strangest grin on his face. We ended up leaving that night without saying too much more. We were engaged on Valentines day.
(Picture taken not long after becoming engaged. I look like I'm correcting his posture.)So, nine years and still not in Fayetteville. That's okay. The trade-off has been worth it!
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