Week 10-12 meds PAT201

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Loop diuretics
Furosemide Indications: HTN, edema d/t HF, hepatic impairment, renal disease Mechanisms of action: Inhibits reabsorption of Na and Cl from the loop of Henle and distal renal tubule Increases renal excretion of water, Na, Cl, Mg, K, Ca Desired effects: Decrease preload Decrease BP Diuresis Adverse effects: More likely to cause severe potassium loss, hypovolemia, and hypotension compared to other diuretic classes Are ototoxic (cause damage to hearing and balance)- an effect more likely to occur in clients with renal insufficiency or high doses of drug administered May also increase glucose and uric acid levels - monitor these lab values during therapy Potassium wasting diuretic
Short-acting thiazide diuretics
Hydrochlorothiazide: Indications: Management of mild-moderate HTN and treatment of edema associated with HF Mechanisms of action: Increases excretion of sodium and water by inhibiting sodium reabsorption in the distal tubule and ascending limb of loop of Henle in kidneys Promotes excretion of chloride, potassium, magnesium, and bicarbonate Desired effects: Decrease in BP Diuresis Decrease preload Adverse effects: Headache, dizziness, orthostatic hypotension, hypokalemia, N/V, GI irritation
Long-acting thiazide-like diuretics
Chlorthalidone: Indications: Management of mild-moderate HTN, treatment of edema associated with HF Mechanisms of action: Increases excretion of Na and water by inhibiting Na reabsorption at the distal tubule Promotes excretion of Cl, K, Mg, and bicarbonate Desired effects: Decreases preload Decreases BP Diuresis Adverse effects: Headache, dizziness, orthostatic hypotension, hypokalemia, N/V, GI irritation
Calcium channel blockers
Nifedipine: Indications: Management of HTN (extended-release only) and angina Mechanisms of action: Selectively blocks calcium channels in myocardial and vascular smooth muscle cells this inhibiting excitation-contraction coupling and subsequent contraction of the heart Desired effects: Decrease in afterload (SVR) Decrease BP Adverse effects: Headache, dizziness, drowsiness, lightheadedness, dysrythmias, N/V, hypotension, tachycardia, palpitations, diarrhea, constipation, nocturia, polyuria
ACE inhibitors
Enalapril: Indications: Management of HF, slows progression of left ventricular dysfunction into overt HF Mechanisms of action: Block conversion of angiotensin 1 to angiotensin 2 resulting in dilation of arterial and venous vessels Decrease renin levels thus decreasing aldosterone levels Prevent degradation of bradykinin and other vasodilatory prostaglandins Net result is systemic vasodilation Desired effects: Decrease preload Decrease afterload (decrease SVR) Decrease BP Decrease development of overt HF Adverse effects: Dizziness, headache, dry cough d/t inhibition of ACE, diarrhea, hypotension, chest pain, tachycardia, dysrythmias, syncope, angina, orthostatic hypotension, hyperkalemia
Losartan Indications: HTN Prevention of stroke in patients with HTN and left ventricular hypertrophy Clients who cannot tolerate ACEIs Mechanisms of action: Selectively blocks binding of angiotensin 2 to the angiotensin 1 receptors Blocks vasoconstricting effects of angiotensin 2 and aldosterone-secreting effects of angiotensin 2 Desired effects: Decrease preload Decrease afterload (SVR) Decrease BP Adverse effects: Dizziness, insomnia, headache, hypotension, diarrhea, constipation, dry mouth, hyperkalemia
A1-adrenergic antagonists
Doxazosin: First dose phenomenon, especially syncope may occur Therefore it is important to assess BP prior to and during therapy Assess for common SE such as weakness, dizziness, headache, N/V Older adults especially prone to hypotensive and hypothermic effects related to vasodilation Indications: HTN Benign prostatic hyperplasia and urinary obstruction because they relax smooth muscle in the prostate and bladder neck, thus reducing urethral resistance Mechanism of action: Dilates arteries and veins by blocking postsynaptic a-1 adrenergic receptors in vascular smooth muscle causing muscle to relax Desired effects: Decrease afterload (SVR) Decrease BP Increase urine flow and decrease sx of BPH Adverse effects: Dizziness, weakness, drowsiness, headache, orthostatic hypotension, palpitations, chest pain, edema, dysrythmias, N/V, diarrhea, constipation, abdominal pain
Beta blockers
Metoprolol Indications: HTN, angina, MI, HF Mechanism of action: Blocks stimulation of beta-1 (myocardial)-adrenergic receptors Does not usually affect beta-2 (pulmonary, vascular, uterine)-adrenergic receptor sites Desired effects: Decreases elevated renin and plasma levels Decrease CO by decreasing HR and decreasing contractility Decreases myocardial O2 demand Decreases BP Decreases frequency of angina Adverse effects: Insomnia, dizziness, headache, HF, palpitations, dysrythmias, cardiac arrest, hypotension, bradycardia, pulmonary/peripheral edema, chest pain, N/V, diarrhea, constipation DO NOT suddenly stop taking as can cause chest pain or MI
Potassium supplements
Potassium chloride Indications: Treatment or prevention of hypokalemia, treatment of mild alkalosis Mechanism of action: Mimics endogenous K ions Desired effects: Maintain K balance Can decrease BP (unknown cause but may be through loss of Na - electroneutrality) Adverse effects: GI: abd pain, N/V, diarrhea, bleeding/ulceration d/t irritation with oral forms Local: pain and irritation at IV site, phlebitis Hyperkalemia
HMG-CoA reductase inhibitors
atorvastatin: First drug of choice for decreasing lipid levels Indications for use: Hypercholesterolemia, elevated triglyceride levels Mechanism of action: Inhibit HMG-CoA reductase, the enzyme needed for cholesterol biosynthesis, so ↓ cholesterol Increase number of LDL receptors on liver cells Desired effects: ↓ cholesterol levels and LDLs, ↑ HDL levels Adverse effects: Headache, abdominal cramps, constipation, diarrhea, heartburn, nausea, rash Interactions: Grapefruit juice inhibits the metabolism of statins; can lead to rhabdomyolysis (breakdown of muscle fibers) where muscle cells spill into systemic circulation, which can clog the kidneys and cause acute renal failure Recommond pt. To not take meds with juice as fruit punch is often mised
amitriptyline Inhibits reuptake of serotonin and NE Indications: Management of pain associated with peripheral artery disease Mechanism of action: correct imbalance of serotonin (5-HT) & NE (inhibitory neurotransmitters) blocks presynaptic reuptake of serotonin (5-HT) & NE so stay in synaptic cleft longer modulates ascending pain impulses thus controls pain transmission in peripheral and CNS serotonin also regulates sleep, mood, appetite, libido Desired effects: ↓pain through modulation ↑serotonin → better sleep, mood, appetite Adverse effects: potent anticholinergic effects i.e., dry mouth, constipation, blurred vision, urinary retention, cardiac dysrhythmias If pt. Has already had heart attack, you may not want to administer this medication, and have careful monitoring through ECG
Antiplatelets: ADP receptor blockers
Clopidogrel: Indications: treatment of arterial thromboembolism, reduce the risk of stroke, MI, TIA Mechanism of action: inhibits ADP receptors on platelets and prolongs bleeding time Pharmacodynamics: ADP (promotes platelet aggregation is one of the chemicals that is released by platelets So ADP receptor blockers alter the plasma membrane of platelets thus platelets are unable to recognize chemical signals required to aggregate Desired effects: decreased possibility of stroke and MI by decreasing platelet aggregation Adverse effects: H/A, dizziness, diarrhea, bruising, bleeding, GI bleeding (cells of GI slough off often so tissues are vulnerable) Monitor for patients with liver failre
COX inhibitors/Antiplatelets: ASA
Acts by binding to the enzyme cyclooxygenase in platelets This binding irreversibly inhibits the formation of thromboxane A2 (powerful inducer of platelet aggregation) Inhibits specific clotting factors Indications: TIAs, ischemic stroke, acute coronary syndrome, secondary prevention of vascular events, treatment of mild-moderate pain and reduces inflammation Mechanism of action: binds to COX and inhibits formation of thromboxane A2 Desired effect: inhibit platelet aggregation, COX irreversibly inhibited by ASA for lifespan of platelet (7-10 days), even if we stop medication it will still be bound to platelet for 7-10 days Adverse effects: Lots of GI effects because COX has protective effects GI bleeds, bruising, nausea, vomiting, Reye’s syndrome NOTE: Aspirin is no longer recommended as primary prevention for first vascular event due to irreversible binding, however is strongly indicated for secondary prevention Recall of what COX enzymes do Arachidonic acid (from phospholipids) Cox 1 (Housing keeping homeostatic functions) Thromboxane (vasoconstriction and increased platelet aggregation (Thrombosis)
Thrombolytics: tPA
Alteplase: For ischemic strokes only, NOT hemorrhagic Mechanism of actions Dissolves clot within blood vessel by activating protein that promotes fibrinolysis, or clot destruction through converting plasminogen to plasmin Plasmin digests fibrin and breaks down fibrinogen, prothrombin, and other plasma proteins and clotting factors Narrow margin of safety, very potent drug, will kill all clots Are nonspecific and will dissolve “abnormal” and “normal” clots More effective when given ASAP after clot formation occurs (within 4hr) Indications: MI and CVA related to clots Mechanism of action: Mimics body’s own tPA which is found in endothelial cells tPA Binds to fibrin component of thrombus Converts plasminogen to plasmin, which then dissolves fibrin clots Desired effects: re-establishes blood flow to prevent further damage Adverse effects: Contraindicated in clients with active bleeding or recent history of trauma Internal and superficial bleeding, intracranial hemorrhage, nose bleeds