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.