Week 10-12 meds PAT201

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

ARBs

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

Antidepressants

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