Week 16 Blog #2

Blog #2:

Week 16 April 18-24
Sunday, April 23, 2016
2p-10p 8 Hours Interned
Wanted to make note that this is the last week I will be blogging related to my internship. The academic semester is technically over on Friday, April 22, 2016 but am still in agreement to intern until April 30, 2016.

3. After being provided with a list of the 12 most commonly prescribed drugs at our facility, Robin will be able to verbally demonstrate knowledge of their pharmacotherapeutics, pharmacodynamics, and adverse effects.

Digoxin

Drug Class – Inotropics.

Therapeutic Class – Cardiac glycoside.

Indications – Heart failure, congestive cardiac insufficiency, arrhythmias, heart failure, paroxysmal supraventricular tachycardia, and atrial fibrillation and flutter.

Pharmacotherapeutics – Digoxin also acts on the electrical activity of the heart, increasing the slope of phase 4 depolarization, shortening the action potential duration, and decreasing the maximal diastolic potential, thus, preventing the diagnoses listed above from occurring.

Pharmacodynamics – Digoxin inhibits the Na-K-ATPase membrane pump, resulting in an increase in intracellular sodium. The sodium calcium exchanger (NCX)in turn tries to extrude the sodium and in so doing, pumps in more calcium. Increased intracellular concentrations of calcium may promote activation of contractile proteins (e.g., actin, myosin).

Adverse Effects – Agitation, fatigue, generalized muscle weakness, hallucinations, dizziness, headache, stupor, vertigo, arrhythmias, heart block, blurred vision, diplopia, light flashes, photophobia, yellow-green halos around vidual images, anorexia, nausea, diarrhea, and vomiting.

Hydrocodone / APAP

Drug Class – Opioid.

Therapeutic Class – Opioid analgesic combination.

Indications – Mild to moderate pain.

Pharmacotherapeutics – Used for pain management.

Pharmacodynamics – Hydrocodone acts as a weak agonist at OP1, OP2, and OP3 opiate receptors within the central nervous system (CNS). Hydrocodone primarily affects OP3 receptors, which are coupled with G-protein receptors and function as modulators, both positive and negative, of synaptic transmission via G-proteins that activate effector proteins. Binding of the opiate stimulates the exchange of GTP for GDP on the G-protein complex. As the effector system is adenylate cyclase and cAMP located at the inner surface of the plasma membrane, opioids decrease intracellular cAMP by inhibiting adenylate cyclase. Subsequently, the release of nociceptive neurotransmitters such as substance P, GABA, dopamine, acetylcholine, and noradrenaline is inhibited. Opioids such as hydrocodone also inhibit the release of vasopressin, somatostatin, insulin, and glucagon. Opioids close N-type voltage-operated calcium channels (OP2-receptor agonist) and open calcium-dependent inwardly rectifying potassium channels (OP3 and OP1 receptor agonist). This results in hyperpolarization and reduced neuronal excitability.

Adverse Effects – Drowsiness, sedation, dizziness, light-headedness,physical dependence, confusion, bradycardia, flushing, hypotension, constipation, dry mouth, nausea, vomiting, urine retention, and respiratory depression.

Latanoprost Eye Drops (Xalatan)

Drug Class – Antiglaucomas.

Therapeutic Class – Prostaglandin analogue.

Indications – For patients with ocular hypertension or open-angle glaucoma.

Pharmacotherapeutics – Decreases intraocular pressure and increases the outflow of aqueous fluid in an individuals eye to prevent the progression of ocular hypertension and/or open-angle glaucoma.

Pharmacodynamics – Latanoprost is a prostaglandin F2a analogue. Specifically, Latanoprost is a prostanoid selective FP receptor agonist that is believed to reduce the intraocular pressure (IOP) by increasing the outflow of aqueous humor. Studies in animals and man suggest that the main mechanism of action is increased uveoscleral outflow. Elevated IOP represents a major risk factor for glaucomatous field loss. The higher the level of IOP, the greater the likelihood of optic nerve damage and visual field loss.

Adverse Effects – Blurred vision, burning, foreign body sensation, increased brown pigmentation of the iris, itching, stinging, conjunctival hyperemia, dry eye, excessive tearing, eye pain, eyelash changes, lid crusting or edema, lid discomfort, photophobia, muscle, joint, or back pain, upper respiratory tract infection, allergic skin reactions, rash, cold, and/or flulike syndrome.

This is my last post guys! Thanks for reading! Hope you learned as much as I did!

Week 16 Blog #1

Blog #1:

Week 16 April 18-24

Saturday, April 23, 2016

2p-10p 8 Hours Interned

Wanted to make note that this is the last week I will be blogging related to my internship. The academic semester is technically over on Friday, April 22, 2016 but am still in agreement to intern until April 30, 2016.

3. After being provided with a list of the 12 most commonly prescribed drugs at our facility, Robin will be able to verbally demonstrate knowledge of their pharmacotherapeutics, pharmacodynamics, and adverse effects.

Klor-con

Drug Class – Potassium supplement.

Therapeutic Class – Potassium saltt.

Indications – Hypokalemia.

Pharmacotherapeutics – Klor Con is used to replenish potassium blood levels in an individual who has hypokalemia. Klor Con is a potassium supplement used to restore normal potassium levels.

Pharmacodynamics – Potassium supplement (electrolyte replenisher); participates in a number of essential physiological processes, including the maintenance of intracellular tonicity, the transmission of nerve impulses, the contraction of cardiac, skeletal, and smooth muscle, and the maintenance of normal renal function.

Adverse Effects – confusion, anxiety, uneven heartbeat, extreme thirst, increased urination, leg discomfort, muscle weakness or limp feeling, hyperkalemia, numbness, tingly feeling in your hands, feet, or around your mouth, diarrhea, stomach pain, vomiting, black, bloody, or tarry stools, hives, difficulty breathing, and swelling of your face, lips, tongue, or throat.

Warfarin (Coumadin)

Drug Class – Anticoagulant.

Therapeutic Class – Coumarin derivative.

Indications – Pulmonary embolism, deep vein thrombosis, MI, rheumatic heart disease with heart valve damage, prosthetic heart valves, and chronic atrial fibrillation.

Pharmacotherapeutics – Inhibits vitamin K-dependent activation of clotting factors II, VII, IX, and X, formed by the liver, thus, preventing the formation of blood clots.

Pharmacodynamics – Warfarin inhibits vitamin K reductase, resulting in depletion of the reduced form of vitamin K (vitamin KH2). As vitamin K is a cofactor for the carboxylation of glutamate residues on the N-terminal regions of vitamin K-dependent proteins, this limits the gamma-carboxylation and subsequent activation of the vitamin K-dependent coagulant proteins. The synthesis of vitamin K-dependent coagulation factors II, VII, IX, and X and anticoagulant proteins C and S is inhibited. Depression of three of the four vitamin K-dependent coagulation factors (factors II, VII, and X) results in decreased prothrombin levels and a decrease in the amount of thrombin generated and bound to fibrin. This reduces the thrombogenicity of clots.

Adverse Effects – Fever, headache, dizziness, fatigue, syncope, angina syndrome, hypotension, hemorrhage, hepatitis, jaundice, cholestatic hepatic injury, dermatitis, urticarial, necrosis, alopecia, rash, hypersensitivity, allergic reactions, and anaphylactic reactions.

Lisinopril (Prinivil or Zestril)

Drug Class – Angiotensin-converting enzyme inhibitor.

Therapeutic Class – ACE Inhibitor.

Indications – Hypertension, symptomatic congestive heart failure, adjunct treatment for heart failure, hemodynamically stable patients within 24 hours of acute MI to improve survival

Pharmacotherapeutics – Lisinopril decreases the production of angiotensin II and suppression of the renin-angiotensin-aldosterone system. In doing so, it increases vasodilation and decreases blood pressure, related to the indicated diagnoses listed above.

Pharmacodynamics – Lisinopril is an orally active ACE inhibitor that antagonizes the effect of the RAAS. The RAAS is a homeostatic mechanism for regulating hemodynamics, water and electrolyte balance. During sympathetic stimulation or when renal blood pressure or blood flow is reduced, renin is released from the granular cells of the juxtaglomerular apparatus in the kidneys. In the blood stream, renin cleaves circulating angiotensinogen to ATI, which is subsequently cleaved to ATII by ACE. ATII increases blood pressure using a number of mechanisms. First, it stimulates the secretion of aldosterone from the adrenal cortex. Aldosterone travels to the distal convoluted tubule (DCT) and collecting tubule of nephrons where it increases sodium and water reabsorption by increasing the number of sodium channels and sodium-potassium ATPases on cell membranes. Second, ATII stimulates the secretion of vasopressin (also known as antidiuretic hormone or ADH) from the posterior pituitary gland. ADH stimulates further water reabsorption from the kidneys via insertion of aquaporin-2 channels on the apical surface of cells of the DCT and collecting tubules. Third, ATII increases blood pressure through direct arterial vasoconstriction. Stimulation of the Type 1 ATII receptor on vascular smooth muscle cells leads to a cascade of events resulting in myocyte contraction and vasoconstriction. In addition to these major effects, ATII induces the thirst response via stimulation of hypothalamic neurons. ACE inhibitors inhibit the rapid conversion of ATI to ATII and antagonize RAAS-induced increases in blood pressure. ACE (also known as kininase II) is also involved in the enzymatic deactivation of bradykinin, a vasodilator. Inhibiting the deactivation of bradykinin increases bradykinin levels and may further sustain the effects of lisinopril by causing increased vasodilation and decreased blood pressure.

Adverse Effects – Dizziness, headache, fatigue, paresthesia, orthostatic hypotension, hypotension, chest pain, nasal conjestion, diarrhea, nausea, dyspepsia, hyperkalemia, dyspnea, dry, persistent, tickling, nonproductive cough, and angioedema.

Week 15 Blog #2

Blog #2:

Week 15 April 11-17

Wanted to make note that I only interned 4 hours this week due to review for finals week. In my internship agreement I am to complete 120 hours during the semester, roughly 8 hours a week, in which I have already surpassed. But I will still be doing my biweekly blog as another requirement to my internship agreement.

3. After being provided with a list of the 12 most commonly prescribed drugs at our facility, Robin will be able to verbally demonstrate knowledge of their pharmacotherapeutics, pharmacodynamics, and adverse effects.

Atorvastatin (Lipitor):

Drug Class – HMG-CoA reductase inhibitor.

Therapeutic Class – Antilipemic.

Indications – Hyperlipidemia and/or hypercholesterolemia. Hyperlipidemia means there is a high concentration of lipids in the blood. Hypercholesterolemia means there is an excess of cholesterol in the bloodstream.

Pharmacotherapeutics – Atovastatin is used to treat high cholesterol levels by reducing the levels of “bad cholesterol” (low-density lipoproteins) and triglycerides in the blood, while increasing the levels of “good cholesterol” (high-density lipoproteins). In doing so, atorvastatin lowers the risk of stroke, heart attack, and other heart complications in people with type two diabetes, coronary heart disease, and/or other risk factors.

Pharmacodynamics – Antilipemics lower elevated blood levels of lipids. Bile-sequencing drugs lower blood levels of low-density lipoproteins by forming insoluble complexes with bile salts, triggering cholesterol to leave the bloodstream and other storage areas to make new bile acids. Fibric acid derivatives reduce cholesterol formation, increase sterol excretion, and decrease lipoprotein and triglyceride synthesis. HMG-COa reductase inhibitors interfere with enzymatic activity that generates cholesterol in the liver. Selective cholesterol absorption inhibitors inhibit cholesterol absorption by the small intestine, decreasing hepatic stores of cholesterol and increasing clearance of cholesterol from the blood.

Adverse Effects – Headache, asthenia, sinusitis, pharyngitis, abdominal pain, constipation, diarrhea, dyspepsia, flatulence, back pain, arthralgia, myalgia, rash, anaphylaxis, angioedema, infection, flulike syndrome, and hypersensitivity reaction.

Omeprazole (Prilosec):

Drug Class – Proton pump inhibitor.

Therapeutic Class – Gastric acid suppressant.

Indications – Erosive esophagitis, gastroesophegeal reflux disease (GERD), GERD without erosive esophagitis, pathologic hypersecretory conditions, duodenal ulcer, gastric ulcer, H. pylori eradication to reduce risk of duodenal ulcer reoccurrence, and heartburn.

Pharmacotherapeutics – Omeprazole is used inhibit acid secretions.

Pharmacodynamics – Omeprazole is a proton pump inhibitor that suppresses gastric acid secretion by specific inhibition of the H⁺/K⁺-ATPase in the gastric parietal cell. By acting specifically on the proton pump, omeprazole blocks the final step in acid production, thus reducing gastric acidity.

Adverse Effects – Headache, dizziness, diarrhea, abdominal pain, nausea, vomiting, constipation, flatulence, back pain, cough, and rash.

Amlodipine (Norvasc):

Drug Class – Calcium channel blocker and/or antianginal.

Therapeutic Class – Cardiovascular agent.

Indications – High blood pressure and angina.

Pharmacotherapeutics – Amlodipine is used to relax blood vessels and increase the supply of blood and oxygen to the heart while reducing the hearts workload, thus, lowering blood pressure and relieving angina.

Pharmacodynamics – Amlodipine decreases arterial smooth muscle contractility and subsequent vasoconstriction by inhibiting the influx of calcium ions through L-type calcium channels. Calcium ions entering the cell through these channels bind to calmodulin. Calcium-bound calmodulin then binds to and activates myosin light chain kinase (MLCK). Activated MLCK catalyzes the phosphorylation of the regulatory light chain subunit of myosin, a key step in muscle contraction. Signal amplification is achieved by calcium-induced calcium release from the sarcoplasmic reticulum through ryanodine receptors. Inhibition of the initial influx of calcium decreases the contractile activity of arterial smooth muscle cells and results in vasodilation. The vasodilatory effects of amlodipine result in an overall decrease in blood pressure. Amlodipine is a long-acting CCB that may be used to treat mild to moderate essential hypertension and exertion-related angina (chronic stable angina). Another possible mechanism is that amlodipine inhibits vascular smooth muscle carbonic anhydrase I activity causing cellular pH increases which may be involved in regulating intracelluar calcium influx through calcium channels

Adverse Effects – Bradycardia, confusion, constipation, depression, diarrhea, dizziness, edema, elevated liver enzyme levels, fatigue, flushing, headache, hypotension, insomnia, nervousness, and rash.

Week 15 Blog #1

Blog #1:

Week 15 April 11-17
Monday, April 11, 2016
4p-8p 4 Hours Interned 

Also want to make note that I will have only interned 4 hours this week and no hours next week due to review for finals week and finals week. In my internship agreement I am to complete 120 hours during the semester, roughly 8 hours a week, in which I have already surpassed. But I will still be doing my biweekly blog as another requirement to my internship agreement.

3. After being provided with a list of the 12 most commonly prescribed drugs at our facility, Robin will be able to verbally demonstrate knowledge of their pharmacotherapeutics, pharmacodynamics, and adverse effects.

Levothyroxine (Synthroid)

Drug Class – Hormone.

Therapeutic Class – Thyroid Hormone Replacement.

Indications – Hypothyroidism. Hypothyroidism means there is a low count of thyroid hormone thyroxine (T4) which is made and released by the thyroid gland.

Pharmacotherapeutics – Levothyroxine is used as replacement hormone therapy in hypothyroidism.

Pharmacodynamics (mechanism of action) – Levothyroxine acts as a replacement hormone for the natural thyroid hormone, T4, made by the thyroid gland. Levothyroxine (T4) is a naturally occurring hormone produced by the thyroid gland and converted to the more active hormone triiodothyronine (T3) in peripheral tissues. The precise signals controlling the conversion of T4 to T3 within the cell are not known. The thyroid hormones are required for normal growth and development, particularly of the nervous system. They increase the resting or basal metabolic rate of the whole organism and have stimulatory effects on the heart, skeletal muscle, liver and kidney. Thyroid hormones enhance lipolysis and the utilization of carbohydrate. Increased oxygen consumption, respiration, heart rate, growth and maturation, and speed of fat, protein, and carbohydrate metabolism occur secondary to increase in the basal metabolic rate.

Adverse Effects – Fever, headache, nervousness, insomnia, tremor, tachycardia, palpitations, arrhythmias, angina, hypertension, cardiac arrest, appetite change, nausea, diarrhea, menstrual irregularities, weight loss, leg cramps, diaphoresis, and heat intolerance.

Furosemide (Lasix)

           

Drug Class – Loop Diuretic.

Therapeutic Class – Diuretic, antihypertensive.

Indications – Edema from heart failure, hepatic cirrhosis, or nephrotic syndrome. Mild to moderate hypertension. And used as adjunct treatment in acute pulmonary edema or hypertensive crisis.

Pharmacotherapeutics – Furosemide is used to manage hypertension and edema associated with CHF, cirrhosis, and renal disease, including nephrotic syndrome.

Pharmacodynamics – Furosemide inhibits sodium and chloride reabsorption in the ascending loop of Henle, thus increasing renal excretion of sodium, chloride, potassium, and water. This is achieved through competitive inhibition at the chloride binding site in the cotransporter, thus, preventing the transport of sodium from the lumen of the loop of Henle into the basolateral interstitium. Consequently, the lumen becomes more hypertonic while the interstitium becomes less hypertonic, which in turn diminishes the osmotic gradient for water reabsorption throughout the nephron. Because the thick ascending limb is responsible for 25% of sodium reabsorption in the nephron, furosemide is a very potent diuretic.

Adverse Effects – Fever, vertigo, headache, dizziness, paresthesia, restlessness, weakness, volume depletion, dehydration, orthostatic hypotension, thrombophlebitis, transient deafness, blurred or yellow vision, abdominal discomfort and pain, diarrhea, anorexia, nausea, vomiting, constipation, pancreatitis, nocturia, polyuria, frequent urination, oliguria, agranulocytosis, leukopenia, thrombocytopenia, azotemia, anemia, aplastic anemia, hepatic dysfunction, hypokalemia, hypochloremic alkalosis, asymptomatic hyperuricemia, gout, fluid and electrolyte imbalances, impaired glucose intolerance, muscle spasm, dermatitis, purpura, and photosensitivity.

Metoprolol (Lopressor or Toprol XL)

Drug Class – Beta Blocker and/or antianginals.

Therapeutic Class – Antihypertensive, adjunct treatment for acute MI.

Indications – For the management of acute myocardial infarction, angina pectoris, heart failure and mild to moderate hypertension. May be used to treat supraventricular and tachyarrhythmias and as prophylaxis for migraine headaches.

Pharmacotherapeutics – Metoprolol is used to decrease heart rate, cardiac output, and blood pressure.

Pharmacodynamics – Metoprolol competes with adrenergic neurotransmitters such as catecholamines for binding at beta(1)-adrenergic receptors in the heart. Beta(1)-receptor blockade results in a decrease in heart rate, cardiac output, and blood pressure.

Adverse Effects – Bradycardia, heart failure, AV block, peripheral vascular disease, cough, diarrhea, disturbing dreams, dizziness, dyspnea, bronchospasm, fatigue, fever, hypotension, lethargy, nausea, peripheral edema, rash, and wheezing.