Diuretics Loop Nursing Considerations PDF

Diuretics: MOA: LOOP DIURETICS Loop diuretics work by blocking the sodium-potassium-chloride (Na⁺/K⁺/2Cl⁻) transporter in the ascending loop of Henle (a part of the kidney). This prevents sodium, potassium, and chloride from being reabsorbed back into the blood, causing more water to stay in...

Diuretics: MOA: LOOP DIURETICS Loop diuretics work by blocking the sodium-potassium-chloride (Na⁺/K⁺/2Cl⁻) transporter in the ascending loop of Henle (a part of the kidney). This prevents sodium, potassium, and chloride from being reabsorbed back into the blood, causing more water to stay in the urine and be excreted ◦block NaCl reabsorption, block reabsorption of water As a result, loop diuretics help reduce fluid buildup (diuresis) in conditions like heart failure, kidney disease, and hypertension. LOOPS AND SPIRONOLACTONE Loop diuretics (like furosemide) and spironolactone are often used together because they balance each other’s effects and enhance diuresis while preventing complications. ◦Preventing Potassium Loss (Balancing Electrolytes) ‣ Loop diuretics remove excess fluid by increasing urine output, but they also cause potassium loss, which can lead to hypokalemia (low potassium). ‣ Spironolactone, a potassium-sparing diuretic, works differently by blocking aldosterone, which helps retain potassium. This prevents potassium loss caused by loop diuretics. ‣ Example: Think of loop diuretics as a faucet draining excess water (and potassium) rapidly, while spironolactone acts like a control valve, making sure the essential potassium isn’t lost. ◦Better Fluid Removal (Stronger Diuretic Effect) ‣ Loop diuretics work in the loop of Henle to remove large amounts of fluid. ‣ Spironolactone works later in the distal tubule and collecting duct to provide a more balanced and prolonged effect. ‣ Together, they provide stronger diuresis while reducing side effects like excessive potassium loss or dehydration. ◦Commonly Used in Conditions Like: ‣ Heart failure: to reduce fluid overload and prevent potassium depletion. ‣ Liver cirrhosis with ascites: spironolactone is preferred, but loop diuretics help remove excess fluid faster. ‣ Resistant hypertension: when blood pressure is hard to control with a single medication. LOOPS: NURSING INTERVENTIONS Monitor Fluid Balance ◦daily weights/I&O's to assess fluid loss. ◦monitor signs of dehydration (dry mouth, hypotn, dizziness, weight loss, oliguria) ‣ administer on intermittent schedule, start on low dose Monitor Electrolytes ◦check potassium levels (risk of hypokalemia). ◦monitor sodium and magnesium levels as loop diuretics can cause imbalances. Assess Vital Signs ◦monitor blood pressure (risk of hypotension due to fluid loss). ‣ discontinue if hypotension is too bad ◦check heart rate/dysrhythmias (irregularities may indicate electrolyte disturbances). ‣ want to avoid taking with digoxin Watch for Ototoxicity (Hearing Loss) ◦high doses or rapid IV infusion can cause tinnitus or hearing damage. ‣ avoid other ototoxic drugs (gentamycin) Monitor for Signs of Hypokalemia ◦muscle cramps, weakness, irregular heartbeat (may need potassium supplements). Administer in the Morning  ◦prevents nocturia (nighttime urination) and disrupted sleep. Caution in pts with DM ◦can cause hyperglycemia Caution in pts with Gout ◦can cause hyperuricemia Patient Education: ◦Take in the Morning ‣ avoid taking it late to prevent waking up frequently to urinate. ◦Change Positions Slowly ‣ to prevent dizziness or falls due to low blood pressure. ◦Eat Potassium-Rich Foods (unless on potassium supplements) ◦Monitor for Dehydration ‣ signs include polydipsia, dry mouth, weakness, or confusion. ◦Recognize Signs of Low Potassium ‣ leg cramps, irregular heartbeat, or muscle weakness. ◦Avoid NSAIDs (like ibuprofen) ‣ they can reduce the effectiveness of loop diuretics. ◦Report Hearing Issues ‣ if ringing in the ears or hearing loss occurs. ◦Follow-Up Labs & Checkups ‣ regular blood tests for electrolytes and kidney function LOOP DIURETICS: SPECIFIC DRUGS Torsemide & Furosemide ◦both are loop diuretics and follow the above MOA and nursing considerations Labs to monitor ◦Electrolytes (especially potassium & sodium) ‣ can cause hypokalemia and hyponatremia. ◦Renal Function (BUN, Creatinine, GFR) ‣ watch for kidney impairment. ◦Liver Enzymes (ALT, AST) ‣ Torsemide is partially metabolized by the liver. ◦Blood Pressure ‣ check for hypotension. ◦Blood Glucose (in diabetics) ‣ can cause hyperglycemia. ◦Uric Acid Levels ‣ may increase and worsen gout. Serious Adverse Effects ◦Ototoxicity ‣ Hearing loss, tinnitus (rare, but risk increases with high doses or rapid IV push). ◦Severe Hypotension & Dehydration ‣ If too much fluid is lost. ◦Renal Failure ‣ If excessive diuresis leads to kidney damage. Why choose Torsemide over Furosemide? ◦More predictable absorption → Works more consistently than furosemide. ◦Longer duration → Requires fewer doses per day (better for long-term use). ◦Liver metabolism → Safer in mild kidney disease (but caution in liver disease). ◦Lower ototoxicity risk → Safer for high-dose or IV use  Why choose Furosemide over Torsemide? ◦Faster elimination → Better for acute fluid overload situations. ◦More widely available → Cheaper and used more commonly. ◦Preferred in severe kidney disease → Since it’s excreted unchanged by the kidneys. MANNITOL: OSMOTIC DIURETIC USE Mannitol is an osmotic diuretic, meaning it works by drawing water out of tissues and into the bloodstream so it can be excreted by the kidneys. This effect is especially useful in conditions with high intracranial pressure (brain swelling) and intraocular pressure (glaucoma). Intracranial Pressure (ICP) ◦Osmotic Effect ‣ Mannitol is a large sugar molecule that stays in the blood. It pulls water from brain tissue into the bloodstream, reducing brain swelling. ◦Decreased Brain Swelling (Edema) ‣ By shifting fluid out of the brain, it lowers pressure inside the skull and prevents further damage. ◦Increased Urine Output ‣ Mannitol is filtered by the kidneys, carrying excess water out and reducing overall body fluid levels. ◦Used for ‣ Brain injuries (trauma, stroke, tumors) ‣ Increased ICP due to cerebral edema Intraocular Pressure (IOP) ◦Pulls Water from the Eye ‣ It reduces fluid buildup in the eye (aqueous humor), lowering pressure inside the eye. ◦Fast-Acting Relief ‣ Used in emergency cases of acute glaucoma attacks before surgery or other treatments. ◦Used for ‣ reserved for patients who have not responded to more conventional treatment ‣ acute glaucoma crisis ‣ before eye surgery to reduce pressure Hemodynamics GOAL OF RAAS SYSTEM Helps regulate blood pressure, fluid balance, and electrolyte levels to maintain homeostasis. Main Goal ◦Increase blood pressure and fluid retention when the body senses low blood volume or low BP How it works ◦Low BP or Low Sodium (Na⁺) Triggers RAAS Activation ‣ Causes the kidneys to release renin (enzyme). ◦Renin Converts Angiotensinogen → Angiotensin I ‣ Angiotensinogen (from the liver) is converted into Angiotensin I. ◦ACE (Angiotensin-Converting Enzyme) Converts Angiotensin I → Angiotensin II ‣ Angiotensin II is the key player that raises BP and conserves fluid by: Vasoconstriction ◦Narrows blood vessels to increase BP. Stimulating Aldosterone Release ◦From the adrenal glands → increases sodium (Na⁺) and water retention,  increasing blood volume. Alteration of Cardiac and Vascular Structure ◦hypertrophy and remodeling Stimulating ADH (Antidiuretic Hormone) ◦From the pituitary → increases water reabsorption in the kidneys. ACE INHIBITORS: MAIN SIDE EFFECTS AND ALTERNATIVE ACE inhibitors (e.g., Lisinopril, Enalapril) block Angiotensin-Converting Enzyme (ACE), which normally breaks down bradykinin. ◦Increased bradykinin leads to cough and, in some cases, angioedema. Dry, persistent cough ◦due to increased bradykinin levels Angioedema ◦rare but life-threatening swelling caused by the accumulation of fluid in the deeper layers of the skin or mucous membranes ◦can lead to difficulty breathing if the swelling affects the airways (such as the tongue, throat, or larynx), which can cause severe respiratory distress. ◦signs of angioedema ‣ swelling around the mouth and neck ‣ dysphagia or dysphonia ‣ stridor What to Use Instead? ◦If a patient develops a cough or angioedema with an ACE inhibitor, switch to: ‣ Angiotensin II Receptor Blockers (ARBs) – Examples: Losartan, Valsartan ◦ARBs do NOT affect bradykinin → No cough or risk of angioedema. ‣ Still effectively lower BP by blocking Angiotensin II at its receptor. HEART FAILURE (R&L) Heart failure is classified based on which side of the heart is failing to pump blood effectively. Left-Sided Heart Failure ("L for Lungs") ◦Blood backs up into the lungs because the left ventricle can’t pump efficiently. ◦Causes pulmonary congestion and respiratory symptoms. ◦Symptoms (Pulmonary/Lung-Related): ‣ Dyspnea (shortness of breath) – Especially during activity or lying down (orthopnea). ‣ Pulmonary edema – Crackles in the lungs, coughing, pink frothy sputum (severe cases). ‣ Paroxysmal Nocturnal Dyspnea (PND) – Waking up gasping for air at night. ‣ Fatigue & Weakness – Poor oxygen delivery to tissues. ‣ Tachycardia & Cool Extremities – The heart tries to compensate, but circulation worsens. ◦Think "L for Left = L for Lungs" – Fluid builds up in the lungs, causing breathing issues. Right-Sided Heart Failure ("R for Rest of the Body") ◦Blood backs up into the systemic circulation because the right ventricle isn’t pumping well. ◦Causes fluid retention and peripheral congestion. ◦Symptoms (Systemic/Fluid Overload): ‣ Peripheral Edema (Swelling) – In the legs, ankles, feet. ‣ Jugular Vein Distension (JVD) – Due to fluid backup in the veins. ‣ Ascites (Abdominal Swelling) – Fluid buildup in the abdomen. ‣ Hepatomegaly & Splenomegaly – Enlarged liver & spleen from blood congestion. ‣ Weight Gain – Due to fluid retention. ◦Think "R for Right = R for Rest of the body" – Fluid builds up in the veins, causing swelling. BETA BLOCKERS Pharmacodynamics ◦Help lower blood pressure (BP) by blocking the effects of norepinephrine (noradrenaline) and epinephrine (adrenaline) on beta-adrenergic receptors. These receptors are primarily located in the heart, lungs, and blood vessels. Beta-blockers are often used for hypertension and other conditions like angina and heart failure. Main Effects on the Heart (β1 Blockade): ◦↓ Heart rate (negative chronotropic effect) ‣ Beta-1 receptors are primarily located in the heart. ‣ When beta-blockers block these receptors, it results in a slower heart rate, which reduces the amount of blood pumped per minute (cardiac output). ‣ Lower cardiac output = lower BP. ◦↓ Contractility (negative inotropic effect) ‣ Beta-1 receptors in the heart also regulate contractility (how strongly the heart contracts). ‣ By blocking these receptors, contractility is reduced, leading to a lower output of blood from the heart and reduced blood pressure. ◦↓ Myocardial oxygen demand ◦↓ Blood pressure (by reducing renin release from kidneys) Some also block β2 receptors (lungs & vessels), leading to ◦Bronchoconstriction (caution in asthma/COPD patients). What Do Beta-Blockers Produce (Clinical Effects)? ◦↓ Heart Rate & Myocardial Workload → Prevents worsening of heart failure. ◦↓ Blood Pressure → Treats hypertension.  ◦↓ Renin Secretion → Reduces RAAS activation (beneficial in heart failure). ◦Anti-arrhythmic Effects → Helps prevent tachyarrhythmias. Beta-blockers slow HR, decrease blood pressure & reduce cardiac workload in heart failure. Beta-blockers reduce BP by: ◦Slowing the heart rate ◦Decreasing the force of contraction ◦Decreasing blood volume (via reduced renin release) Are often combined with vasodilators (diuretics, ACE inhibitors, Dihydropyridine CCB) to ◦Combat reflex tachycardia ◦improve symptoms of HF ◦reduce hospitalizations RAAS Drugs ACE INHIBITORS & CARDIAC REMODELING: Play a critical role in the management of myocardial infarction (MI) and cardiac remodeling. Cardiac Remodeling After MI: ◦cardiac remodeling refers to the changes that occur in the heart after an MI, where the heart's structure and function alter in response to injury. ‣ acute injury (from MI) causes the myocardium (heart muscle) to become stiff, dilated, and weakened over time, impairing its ability to pump blood effectively. ‣ this can lead to left ventricular dysfunction, heart failure, arrhythmias, and worsening clinical outcomes. How ACE Inhibitors Help: ◦Block Angiotensin II Production ‣ After an MI, the RAAS (Renin-Angiotensin-Aldosterone System) is activated. Angiotensin II is a potent vasoconstrictor and causes: Vasoconstriction (raises blood pressure and increases the heart's workload). Release of aldosterone (causes sodium and water retention, contributing to fluid overload). ‣ ACE inhibitors block the conversion of Angiotensin I to Angiotensin II, reducing its harmful effects on the heart and blood vessels. ◦Reduce Afterload ‣ By blocking Angiotensin II, ACE inhibitors help dilate blood vessels, which lowers afterload (resistance the heart works against), making it easier for the heart to pump blood. ‣ This can improve left ventricular function and prevent further damage to the heart after the MI. ◦Prevent Myocardial Hypertrophy & Fibrosis ‣ Angiotensin II stimulates fibrosis (scar tissue formation) and hypertrophy (thickening of the heart muscle), which worsen remodeling. ‣ ACE inhibitors reduce this fibrotic remodeling, helping maintain better heart muscle structure and function. ◦Improve Survival & Outcomes ‣ ACE inhibitors can significantly reduce mortality after an MI, especially in patients with left ventricular dysfunction, by slowing down the progression of heart failure and preventing recurrent heart attacks. Clinical Benefits Post-MI: ◦Prevent further remodeling: Reduces the dilation of the left ventricle and wall thinning, improving overall heart function. ◦Improve ejection fraction: Increases cardiac output and circulatory efficiency, which benefits the entire body.  ◦Reduce risk of heart failure: By controlling the RAAS and preventing fluid retention, ACE inhibitors help avoid heart failure in the post-MI period. ◦Prevent arrhythmias: They help stabilize the heart’s electrical conduction, lowering the risk of arrhythmic events. Post-MI Treatment Strategy: ◦ACE inhibitors (Lisinopril, Ramipril) ‣ prevent cardiac remodeling and reduce mortality. ◦Beta-blockers (Metoprolol) ‣ slow the heart rate and reduce oxygen demand. ◦Aspirin and Antiplatelets ‣ prevent thrombus formation. ◦Statins (Atorvastatin) ‣ lower cholesterol and reduce inflammation in the arteries. ◦Aldosterone antagonists (e.g., Spironolactone) ‣ in patients with heart failure to further reduce cardiac strain. TLDR: ◦ACE inhibitors are essential after MI because they reduce cardiac remodeling, lower blood pressure, and improve heart function, ultimately improving survival and quality of life. ◦They’re often used in combination with other medications like beta-blockers, diuretics, and antiplatelet agents to optimize recovery and reduce the risk of further complications. TYPES OF HYPERTENSION AND HOW TO TREAT Hypertension is classified into two main types: ◦Primary Hypertension (90-95% of cases) has no clear cause and requires lifelong medication to manage blood pressure and prevent complications. ◦Secondary Hypertension (5-10% of cases) has an identifiable cause (e.g., kidney disease, hormonal disorders) and may be reversible if the cause is treated. Drug Therapy: ◦Primary Hypertension: Managed with ACE inhibitors, ARBs, calcium channel blockers, diuretics, or beta-blockers. ◦Secondary Hypertension: Same drugs may be used, but treatment focuses on fixing the underlying cause (e.g., surgery for adrenal tumors, treating kidney disease). Duration: ◦Primary Hypertension: Lifelong treatment is needed. ◦Secondary Hypertension: Temporary or long-term, depending on whether the cause is curable ‣ HTN could be primary or secondary to HF, but remodeling is not reversible so they will be on lifelong treatment regimen Calcium Channel Blockers COMBINATION THERAPY: NIFEDIPINE AND BETA BLOCKERS (METOPROLOL) Prevents Reflex Tachycardia ◦Nifedipine (a dihydropyridine CCB) causes vasodilation, which can lead to a drop in blood pressure. ‣ The body compensates by activating the sympathetic nervous system (SNS), leading to reflex tachycardia (fast heart rate). ◦Metoprolol (a beta-blocker) prevents this by blocking beta-1 receptors in the heart, keeping the heart rate stable. Enhances Blood Pressure Control ◦Nifedipine works on blood vessels (vasodilation), reducing afterload. ◦Metoprolol works on the heart, decreasing cardiac output and sympathetic activation. ◦Together, they provide better BP control than using either alone. Reduces Myocardial Oxygen Demand (Good for Angina/Coronary Artery Disease) ◦Nifedipine lowers vascular resistance, improving oxygen delivery. ◦Metoprolol slows heart rate and reduces contractility, lowering oxygen demand and preventing ischemia. Prevents Worsening of Cardiac Workload ◦If Nifedipine is used alone, the increase in heart rate can strain the heart, especially in patients with coronary artery disease (CAD). ◦Metoprolol balances this effect by keeping the heart rate controlled. NON-DIHYDROPYRIDINE VS DIHYDROPYRIDINE CCB'S Dihydropyridine CCBs ("-dipine") ◦All end in "-dipine" (e.g., Amlodipine, Nifedipine, Felodipine). ◦work on VSM ◦Primary Effects: ‣ Strong vasodilation → Reduces blood pressure by relaxing vascular smooth muscle. ‣ Minimal effect on heart rate (but can cause reflex tachycardia). ‣ decrease contractile force ‣ Used mainly for hypertension and angina. ◦Key Drugs: ‣ Nifedipine (used for HTN, angina, and Raynaud’s). ‣ Amlodipine (longer-acting, preferred for HTN). ‣ Felodipine, Nicardipine, Clevidipine (used in critical care for BP control). Non-Dihydropyridine CCBs (Verapamil & Diltiazem) ◦two main drugs: Verapamil & Diltiazem. ◦work on VSM & heart ◦Primary Effects: ‣ Work on both the heart and blood vessels.  ‣ Slow heart rate & decrease contractility → Used for arrhythmias (AFib, SVT). ‣ Mild vasodilation (less potent than dihydropyridines). ‣ NO reflex tachycardia because they slow HR. ◦Key Drugs: ‣ Verapamil → Strongest effect on the heart (used for arrhythmias & angina). ‣ Diltiazem → Balanced heart & vascular effects (used for HTN, AFib, and angina). VERAPAMIL SIDE EFFECTS & INTERACTIONS Constipation occurs frequently and is the most common complaint. ◦minimized by increasing dietary fluids and fiber Other common effects—dizziness, facial flushing, headache, and edema of the ankles and feet— occur secondary to vasodilation. Must be used with special caution in patients with cardiac failure, and it must not be used at all in patients with sick sinus syndrome or second-degree or third-degree AV block. In older patients, CCBs have been associated with chronic eczematous eruptions typically starting 3 to 6 months after treatment onset Avoid grapefruit juice Verapamil increases plasma levels of digoxin by about 60%, thereby increasing the risk of digoxin toxicity. If signs of toxicity appear, the digoxin dosage should be reduced. Beta blockers and IV verapamil should be administered several hours apart. Overdose can produce severe hypotension and cardiotoxicity ◦Verapamil can be removed from the gastrointestinal (GI) tract with gastric lavage followed by activated charcoal. IV calcium gluconate can counteract both vasodilation and negative inotropic effects but will not reverse AV block. CCB'S MOA: WHERE THEY WORK The Heart (Myocardium & SA/AV Nodes) → ↓ Contractility & HR ◦Non-dihydropyridines (Verapamil & Diltiazem) work here. ◦Blocking calcium channels in the myocardium (heart muscle) → Reduces contractility (negative inotropic effect). ◦Blocking calcium in the SA node → Slows heart rate (negative chronotropic effect). ◦Blocking calcium in the AV node → Slows conduction (negative dromotropic effect), helping with arrhythmias (AFib, SVT). Vascular Smooth Muscle (Arteries) → Vasodilation & ↓ BP ◦Dihydropyridines (-dipines like Amlodipine, Nifedipine) work here. ◦Blocking calcium relaxes arterial smooth muscle, causing vasodilation → Lowers BP  (afterload reduction). ◦Minimal effect on veins, so no major effect on preload. ◦Can cause reflex tachycardia due to BP drop. Coronary Arteries → Increased Blood Flow to the Heart ◦Both Dihydropyridines & Non-Dihydropyridines work here. ◦Blocking calcium causes coronary vasodilation, increasing oxygen supply to the heart. ◦Used in angina & coronary artery disease (CAD) to prevent ischemia. Dihydropyridines (Amlodipine, Nifedipine) can trigger reflex tachycardia, so they are often combined with beta-blockers. Non-dihydropyridines (Verapamil, Diltiazem) directly suppress heart rate, so reflex tachycardia does not occur Vasodilators HYPERTENSIVE CRISIS FIRST LINE TX Sodium Nitroprusside IV infusion Potent rapid acting vasodilator, venous and arterial When the infusion is stopped, blood pressure returns to pretreatment levels in minutes. Nitroprusside can trigger retention of sodium and water; furosemide can help counteract this effect. Thiazide diuretics are first choice for regular hypertension SIDE EFFECTS OF VASODILATORS Vasodilators (e.g., Nitroglycerin, Nitroprusside, Hydralazine) are commonly used to treat conditions like hypertension, heart failure, and angina. One of their main side effects is orthostatic hypotension, which occurs when a person’s blood pressure drops significantly when they stand up, causing dizziness or fainting. Patient education can include ◦Rise Slowly from Sitting or Lying Position ‣ Encourage patients to stand up slowly from a lying or sitting position to prevent sudden BP drops. ‣ Teach the "sit and stand" technique: First sit up on the edge of the bed for a few seconds, then stand slowly. ◦Increase Fluid Intake ‣ Stay hydrated to help maintain blood volume and support blood pressure. ‣ Limit alcohol consumption, as it can worsen hypotension. ◦Avoid Hot Showers or Baths ‣ Hot water can dilate blood vessels and further lower BP, leading to dizziness. Use lukewarm water instead. ◦Wear Compression Stockings ‣ Encourage the use of compression stockings to help prevent pooling of blood in the legs and improve circulation, reducing the risk of hypotension. ◦Monitor Blood Pressure Regularly ‣ Teach patients to check their BP regularly and report if they notice a significant drop, especially when changing positions. ‣ Note any dizziness or lightheadedness to identify when hypotension is a concern. ◦Small, Frequent Meals ‣ Large meals can sometimes contribute to hypotension, so eating smaller, more frequent meals may help prevent postprandial hypotension (a drop in BP after eating). WHERE DO VASODILATORS WORK Arterioles  ◦Effect ‣ Decreased systemic vascular resistance (afterload) ◦Outcome ‣ Reduces blood pressure by dilating the small arteries and arterioles, which lowers the resistance the heart has to pump against. ‣ Helps treat hypertension and heart failure by making it easier for the heart to pump blood. Veins ◦Effect ‣ Decreased venous return (preload) ◦Outcome ‣ Reduces the amount of blood returning to the heart, decreasing preload (the volume of blood in the heart before it contracts). ‣ This lowers the workload of the heart, which is helpful in heart failure and angina. ‣ Nitroglycerin, for example, works mainly on veins to reduce pulmonary edema and chest pain in angina. Coronary Vessels (Heart's Blood Supply) ◦Effect ‣ Increased blood flow to the heart ◦Outcome ‣ Dilates coronary arteries, improving oxygen delivery to the heart muscle. ‣ Relieves chest pain (angina), as it helps increase oxygen supply to areas of the heart that might be ischemic due to coronary artery disease (CAD). Drugs For Hypertension FIRST LINE TX OF HYPERTENSION Thiazide Diuretics (Hydrochlorothiazide) MOA: Promote sodium and water excretion, which reduces blood volume and thus lowers blood pressure. Benefits: Inexpensive, effective, and can also help reduce the risk of stroke and heart failure. Side Effects: Electrolyte imbalances (low potassium, magnesium), gout flare-ups, increased blood sugar. Cant be used in pts with renal failure Take with meals LIFESTYLE MODIFICATIONS Before starting medication, the following lifestyle changes are recommended for all patients with hypertension: ◦Dietary changes (e.g., DASH diet – high in fruits, vegetables, and low-fat dairy) ◦Weight loss (if overweight or obese) ◦Increased physical activity (at least 30 minutes most days of the week) ◦Limit alcohol intake ◦Quit smoking ◦Reduce sodium intake ◦Manage stress ACE INHIBITORS FOR HTN IN KIDNEY PTS ACE inhibitors are commonly preferred for treating hypertension in patients with kidney disorders due to their protective effects on the kidneys. Here's why: ACE Inhibitors and Renal Protection ◦Mechanism of Action (MOA): ACE inhibitors work by blocking the enzyme that converts angiotensin I to angiotensin II, which results in vasodilation (widening of blood vessels) and decreased aldosterone secretion.  ◦Angiotensin II, in particular, has harmful effects on the kidneys, including: ‣ Constriction of the efferent arterioles in the kidneys (the small blood vessels leaving the glomerulus). This increases glomerular pressure and can contribute to kidney damage. ‣ Increased sodium and water retention, which can lead to higher blood pressure and fluid overload. ◦ACE inhibitors prevent this constriction of the efferent arteriole, lowering glomerular pressure and reducing kidney damage over time. They also help reduce proteinuria (protein in the urine), which is an indicator of kidney damage, especially in conditions like diabetic nephropathy. ACE Inhibitors Help Control Blood Pressure ◦Chronic hypertension is a major risk factor for kidney damage and can worsen existing kidney disease. By lowering blood pressure, ACE inhibitors help reduce glomerular hyperfiltration and minimize damage to the nephrons (functional units of the kidney). ◦Lowering blood pressure also helps prevent further progression of kidney damage, especially in patients with conditions like chronic kidney disease (CKD) or diabetic nephropathy. Beneficial Effects in Diabetic Nephropathy ◦Diabetes is a leading cause of kidney disease. In diabetic patients, ACE inhibitors: ◦Reduce glomerular hypertension by dilating the efferent arterioles. ◦Decrease albuminuria (protein in the urine), a key indicator of kidney dysfunction. ACE inhibitors have been shown to reduce the progression of diabetic nephropathy and the need for dialysis. Risk Reduction for Heart Failure and Kidney Disease ◦In patients with heart failure and chronic kidney disease, ACE inhibitors help lower blood pressure, reduce fluid retention, and decrease strain on the heart. This dual effect protects both the heart and kidneys, making ACE inhibitors especially beneficial in these populations. Benefits Over Other Antihypertensive Medications ◦Thiazide diuretics, beta-blockers, and calcium channel blockers are also used to treat hypertension, but they don't offer the same renal protective effects as ACE inhibitors. ◦ARBs (Angiotensin II Receptor Blockers) also offer similar renal protection without the cough side effect, and they are often used in patients who can't tolerate ACE inhibitors. TLDR ◦ACE inhibitors are preferred in patients with kidney disorders because they protect the kidneys by lowering glomerular pressure, reducing proteinuria, and helping control hypertension. ◦They are especially useful in diabetic nephropathy, chronic kidney disease (CKD), and heart failure with kidney involvement. TWO DRUG COMBINATION TX FOR HTN ACE Inhibitor or ARB + Thiazide Diuretic ◦Examples ‣ Lisinopril + Hydrochlorothiazide (HCTZ) ‣ Losartan + HCTZ ◦Why? ‣ ACEi/ARB: Lowers BP, reduces vasoconstriction ‣ Thiazide: Increases sodium/water excretion → lowers BP further ◦Who benefits? ‣ General population, especially Black patients (Thiazides work well) ACE Inhibitor (ACEi) OR ARB + Calcium Channel Blocker (CCB) ◦Examples: ‣ Lisinopril + Amlodipine ‣ Losartan + Nifedipine ◦Why?  ‣ ACEi/ARB: Vasodilation, blocks RAAS ‣ CCB: Vasodilation, reduces arterial resistance ◦Who benefits? ‣ Most effective in Black patients and elderly patients Thiazide Diuretic + Calcium Channel Blocker (CCB) ◦Examples: ‣ HCTZ + Amlodipine ◦Why? ‣ Thiazide: Decreases blood volume ‣ CCB: Relaxes blood vessels ◦Who benefits? Alternative for those who can't take ACE inhibitors/ARBs AVOID These Combinations ◦❌ ACE Inhibitor + ARB → Increases risk of hyperkalemia, kidney damage, and hypotension ◦❌ Beta-blocker + Non-dihydropyridine CCB (Verapamil, Diltiazem) → Risk of bradycardia, heart block Drugs For Heart Failure ENALAPRIL Drug Class: ACE Inhibitor Used to treat hypertension (HTN), heart failure (HF), and kidney protection in diabetic nephropathy. Lab Monitoring for Enalapril ◦Potassium (K⁺) → Can cause hyperkalemia (due to decreased aldosterone production). ◦ Renal Function (Creatinine, BUN, eGFR) → Can cause acute kidney injury (AKI), especially in patients with chronic kidney disease (CKD) or if used with NSAIDs/diuretics (risk of prerenal AKI). ◦Blood Pressure → Risk of hypotension, especially after the first dose. ◦Liver Enzymes (if needed) → Rare risk of liver dysfunction. Enalapril’s Role in Heart Failure (HF) ◦Reduces afterload & preload → Decreases workload on the heart by promoting vasodilation. ◦Inhibits RAAS → Lowers angiotensin II, preventing vasoconstriction and reducing fluid retention. ◦Prevents cardiac remodeling → Protects the heart from further damage and improves survival in HF patients. ◦Used in HF with reduced ejection fraction (HFrEF) → Helps increase cardiac output. Important Considerations in HF Patients: ◦Monitor for hypotension → Start with a low dose and titrate up. ◦Check kidney function regularly → Risk of worsening renal function in HF. ◦Watch for hyperkalemia → Caution with potassium-sparing diuretics (Spironolactone). SPIRONOLACTONE Drug Class: potassium-sparing diuretic and an aldosterone antagonist. Used for hypertension (HTN), heart failure (HF), edema, and conditions like hyperaldosteronism. Side Effects: ◦Hyperkalemia → Can cause dangerously high potassium levels, leading to arrhythmias. ◦Gynecomastia (breast enlargement in men) → Due to its anti-androgen effects.  ◦Menstrual irregularities → Can affect hormone levels. ◦Dehydration & Hypotension → Excessive diuresis can lead to dizziness, low BP. ◦GI disturbances → Nausea, vomiting, diarrhea. ◦Metabolic acidosis → Due to potassium retention. Lab Monitoring & Patient Education ◦Potassium (K⁺) Levels → Monitor frequently due to risk of hyperkalemia (especially if on ACE inhibitors, ARBs, or potassium supplements). ◦Kidney Function (Creatinine, BUN, eGFR) → Avoid in renal failure (risk of worsening kidney function). ◦Sodium Levels → Can cause hyponatremia. ◦Blood Pressure → Monitor for hypotension, especially when used with other diuretics or antihypertensives. Patient Education Tips: ◦Avoid high-potassium foods (e.g., bananas, oranges, potatoes). ◦Watch for signs of high potassium (e.g., muscle weakness, irregular heartbeat). ◦Take in the morning to avoid nocturia. ◦Report hormonal changes (e.g., breast tenderness, irregular periods, hirstuism). ◦Monitor BP regularly at home. HF CLASSES Although classes are helpful in dx and tx of HF, we have to treat the pts sx first, even if their labs say that they are at an earlier stage of HF Sx over labs FIRST LINE TX OF HF ACE Inhibitors (ACEi) OR ARBs (Angiotensin II Receptor Blockers) ◦Examples: Lisinopril, Enalapril, Ramipril (ACEi) / Losartan, Valsartan (ARB) ◦Why? → Reduces afterload/preload, prevents cardiac remodeling, and improves survival. ◦Alternative: ARNI (Sacubitril/Valsartan) for patients who can’t tolerate ACEi/ARB alone. Beta-Blockers (BBs) ◦Examples: Metoprolol succinate, Carvedilol, Bisoprolol ◦Why? → Reduces heart rate, decreases myocardial oxygen demand, and improves survival. ◦Caution: Start low dose, avoid in acute decompensated HF. Diuretics (Loop or Thiazide) – For symptom relief ◦Examples: Furosemide, Torsemide, Hydrochlorothiazide ◦Why? → Reduces fluid overload, pulmonary congestion, and edema. ◦Loop diuretics preferred for severe HF. Aldosterone Antagonists (Potassium-Sparing Diuretics) ◦Examples: Spironolactone, Eplerenone ◦Why? → Blocks aldosterone, reduces fluid retention, improves survival. ◦Monitor potassium (risk of hyperkalemia). ARNI (Angiotensin Receptor-Neprilysin Inhibitor) ◦Example: Sacubitril/Valsartan ◦Why? → Preferred over ACEi/ARB in some HF patients to improve survival and reduce hospitalizations. Antidysrhythmic Drugs PROARRHYTHMIC EFFECTS Proarrhythmic refers to a paradoxical effect where a medication meant to treat arrhythmias (irregular heartbeats) actually causes or worsens them. Antidysrhythmic drugs alter ion channels (Na⁺, K⁺, Ca²⁺) or affect automaticity and conduction velocity, which can sometimes: ◦Prolong repolarization → Increases risk of Torsades de Pointes (TdP) (a life-threatening ventricular arrhythmia). ◦Slow conduction too much → Can cause bradycardia or heart block. ◦Increase ectopic activity → May trigger new arrhythmias instead of suppressing them. Class IA (e.g., Quinidine, Procainamide, Disopyramide) ◦Effect: Prolongs QT interval ◦Risk: Torsades de Pointes, ventricular tachycardia Class IC (e.g., Flecainide, Propafenone) ◦Effect: Strong Na⁺ channel blockade → slows conduction ◦Risk: Can worsen or create new arrhythmias, especially in patients with structural heart disease Class III (e.g., Amiodarone, Dofetilide, Sotalol, Ibutilide) ◦Effect: Prolongs repolarization (K⁺ channel blockade) ◦Risk: Torsades de Pointes (except Amiodarone, which has lower risk) Class IV (e.g., Verapamil, Diltiazem) ◦Effect: Blocks Ca²⁺ channels, slowing AV conduction ◦Risk: Bradycardia, AV block, worsening of heart failure Key Takeaways for Nursing & Monitoring ◦Monitor ECG closely for QT prolongation or new arrhythmias. ◦Check electrolytes (K⁺, Mg²⁺, Ca²⁺) → imbalances increase risk of proarrhythmia. ◦Use caution in structural heart disease (MI, HF) → Class IC is contraindicated. ◦Educate patients on symptoms of worsening arrhythmias (e.g., palpitations, dizziness, syncope). TX AFIB WITH RVR Both beta-blockers (BBs) and calcium channel blockers (CCBs) are used to slow the heart rate and manage symptoms, but they act through different mechanisms. The choice of drug depends on the patient’s overall health, comorbidities, and tolerance. Beta-Blockers (BBs) ◦Why Use Beta-Blockers for AFib with RVR? ‣ Mechanism of Action: Beta-blockers block beta-1 adrenergic receptors in the heart, reducing heart rate by decreasing automaticity and conduction through the AV node. ◦Effects: ‣ Reduce heart rate by slowing AV nodal conduction. ‣ Decrease myocardial oxygen demand (useful in patients with heart disease). ◦Preferred for: ‣ Patients with hypertension, ischemic heart disease, or heart failure. ‣ Esmolol is preferred in acute settings due to its short half-life, allowing for quick adjustments. Calcium Channel Blockers (CCBs) ◦Why Use Calcium Channel Blockers for AFib with RVR? ‣ Mechanism of Action: CCBs block L-type calcium channels in the AV node, reducing calcium influx, which slows conduction and reduces the ventricular response rate. ◦Effects: ‣ Decrease heart rate by slowing AV nodal conduction.  ‣ Diltiazem and verapamil both provide rate control without the side effects seen in beta- blockers. ◦Preferred for: ‣ Patients without heart failure or those with contraindications to beta-blockers (e.g., asthma, bradycardia). ‣ Diltiazem is often used when beta-blockers are not suitable or in non-cardiac patients. Which to Choose? ◦Beta-Blockers (BBs) are preferred in patients with: ‣ Heart failure, especially with reduced ejection fraction (HFrEF) or ischemic heart disease. ‣ Hypertension as part of comprehensive management. ◦Calcium Channel Blockers (CCBs) are preferred in patients with: ‣ Normal left ventricular function or no heart failure. ‣ Asthma or chronic obstructive pulmonary disease (COPD) (since CCBs do not cause bronchoconstriction like beta-blockers). ‣ Acute settings, where rapid rate control is needed and the patient is not in heart failure. TX OF SEVERE VENTRICULAR DYSRHYTHMIAS (VTACH/VFIB) Amiodarone (Class III Antiarrhythmic) ◦First-line drug for stable ventricular tachycardia (VT) and VF (especially in shockable rhythms). ◦Mechanism of Action: ‣ Prolongs action potential duration and refractory period by blocking K⁺ channels, inhibiting Na⁺ and Ca²⁺ channels, and beta-adrenergic blockade. ‣ Slows heart rate and decreases myocardial oxygen demand. ◦Why Amiodarone? ‣ Effective for both ventricular tachycardia (VT) and ventricular fibrillation (VF). ‣ Proven in resuscitation protocols for both pulseless VT and VF. ‣ Can be used intravenously or orally for long-term maintenance after conversion. ◦Amiodarone is preferred because it stabilizes the heart’s electrical activity and has a low risk of proarrhythmia compared to other antiarrhythmic drugs. DIGOXIN DRUG INTERACTIONS Amiodarone (Class III Antiarrhythmic) ◦Interaction: Amiodarone increases digoxin levels by inhibiting the P-glycoprotein (P-gp) and CYP3A4 enzymes, which normally help eliminate digoxin. ◦Effect: Increased digoxin concentration → Risk of digoxin toxicity (e.g., nausea, vomiting, visual disturbances, arrhythmias). ◦Management: ‣ Reduce digoxin dose by 25-50% when starting amiodarone. ‣ Monitor digoxin levels closely, especially after initiating or changing amiodarone dose. Quinidine (Class 1A Antiarrhythmic) ◦Interaction: Quinidine increases digoxin levels by displacing digoxin from tissue-binding sites and inhibiting renal clearance. ◦Effect: Elevated digoxin levels, leading to toxicity (e.g., bradycardia, arrhythmias). ◦Management: ‣ Monitor digoxin levels frequently when starting or adjusting quinidine. ‣ Reduce digoxin dose by 25-50% as needed. Verapamil (Non-dihydropyridine CCB) ◦Interaction: Verapamil increases digoxin levels through P-glycoprotein inhibition and CYP3A4 inhibition. ◦Effect: Digoxin toxicity is more likely, especially when the two drugs are used concurrently, due to slower digoxin elimination. ◦Management:  ‣ Monitor digoxin levels regularly. ‣ Adjust digoxin dose accordingly to prevent toxicity. Diltiazem (Non-dihydropyridine CCB) ◦Interaction: Similar to verapamil, diltiazem can increase digoxin levels through P-glycoprotein inhibition. ◦Effect: Risk of digoxin toxicity, especially in patients with renal impairment or those taking higher doses. ◦Management: ‣ Monitor digoxin levels and adjust the dose of digoxin. ‣ Use with caution and avoid excessive doses of diltiazem. Flecainide (Class 1C Antiarrhythmic) ◦Interaction: Flecainide increases digoxin levels by decreasing renal clearance of digoxin. ◦Effect: Elevated digoxin concentration, which may lead to toxicity. ◦Management: ‣ Monitor digoxin levels when initiating or adjusting flecainide dose. ‣ Consider dose reduction of digoxin if necessary. Sotalol (Class III Antiarrhythmic) ◦Interaction: Sotalol increases the risk of digoxin toxicity due to its effects on the QT interval and heart rate. ◦Effect: The combined use of sotalol and digoxin can increase the risk of arrhythmias and digoxin toxicity. ◦Management: ‣ Monitor ECG and digoxin levels. ‣ Consider alternative therapies for rate control in patients with AF and heart failure. Cholesterol and Triglyceride Drugs THERAPEUTIC LIFESTYLE CHOICES Remember: Therapeutic lifestyle choices (TLCs) first and then drug therapy but always TLC regardless of initiation of drug therapy! STATIN THERAPY Statins are commonly prescribed to lower cholesterol and reduce the risk of cardiovascular events. While statins are generally well tolerated, they can have serious side effects, one of the most concerning being hepatotoxicity (liver damage). Patients on statin therapy may experience symptoms related to liver dysfunction. These symptoms may indicate hepatotoxicity and require prompt medical attention. They include: ◦Jaundice (yellowing of the skin and/or eyes) ‣ This is a key sign of liver dysfunction and indicates bilirubin buildup due to poor liver function. ◦Dark Urine ‣ Dark or tea-colored urine can be a sign of bilirubin being excreted in the urine, suggesting liver damage. ◦Abdominal Pain (especially in the upper right quadrant) ‣ Pain in the upper right abdomen may indicate inflammation or swelling of the liver or gallbladder. ◦Nausea and Vomiting ‣ Persistent nausea, often associated with loss of appetite, may indicate liver distress. ◦Fatigue ‣ Unexplained, prolonged fatigue can result from liver dysfunction or general malaise. ◦Muscle Weakness or Pain (Myopathy) ‣ While muscle pain (myopathy) is not always linked to the liver, it is a common side effect of statins and can coexist with hepatotoxicity.  ◦If muscle pain or weakness is severe and accompanied by dark urine, it may suggest rhabdomyolysis, a severe muscle breakdown that can affect kidney function and liver health. Timing of administration ◦Most statins work best when taken at night, because: ‣ Cholesterol production peaks at night: The liver produces the majority of cholesterol during sleep, and statins are more effective in blocking the enzyme HMG-CoA reductase, which is responsible for cholesterol production, during this period. ‣ Shorter half-life statins (e.g., Simvastatin, Lovastatin): These statins have a shorter half-life, meaning they are processed by the body more quickly. Taking them at night helps ensure they’re working during the peak of cholesterol synthesis. ‣ Longer half-life statins (e.g., Atorvastatin, Rosuvastatin): These statins have a longer duration of action, so they can be taken at any time of the day, although taking them in the evening is still common practice. Their effect on cholesterol production lasts throughout the day. Key Points for Patient Education ◦Take statins at the same time every day: ‣ Establishing a consistent routine helps ensure the medication is taken as prescribed and improves patient adherence. ◦Nighttime administration for short-half life statins: ‣ For Simvastatin and Lovastatin, taking them in the evening enhances their cholesterol- lowering effects because they work best when cholesterol production is at its peak overnight. ◦Don't skip doses ‣ Skipping a dose can reduce the drug's ability to effectively lower cholesterol and may cause unwanted fluctuations in cholesterol levels. ◦Avoid taking with grapefruit (for certain statins): ‣ Grapefruit can interfere with the metabolism of statins, particularly Simvastatin and Lovastatin, by inhibiting the enzyme CYP3A4. This can increase statin levels, raising the risk of side effects such as muscle pain or rhabdomyolysis. PLASMA LIPOPROTEINS AND ASCVD Low-Density Lipoprotein (LDL), commonly referred to as "bad cholesterol". When there is an excess of LDL in the bloodstream, it can accumulate and deposit cholesterol in the walls of arteries, leading to the formation of plaques (atherosclerosis). These plaques can narrow and harden the arteries, increasing the risk of heart attack, stroke, and other cardiovascular events. ◦High LDL levels are strongly associated with an increased risk of atherosclerosis, which is a precursor to many cardiovascular diseases, including coronary artery disease (CAD), heart attacks, and strokes. Reducing LDL levels through lifestyle changes (e.g., diet, exercise) and medications like statins can significantly lower the risk of ASCVD. Drugs for Angina Pectoris SUBLIGUAL NITROGLYCERIN Place the tablet under the tongue and allow it to dissolve completely. Do not chew or swallow the tablet, as it must be absorbed through the mucous membranes under the tongue for fast action. The tablet typically takes 1-2 minutes to dissolve and begin working. If the chest pain does not improve within 5 minutes after the first dose, a second dose can be taken. Take no more than 3 doses in a 15-minute period. Timing of Administration:  ◦Sublingual nitroglycerin should be taken immediately at the onset of chest pain to relieve symptoms quickly. ◦It may also be prescribed for use before activities that could trigger angina, such as physical exertion or emotional stress, to prevent an attack. After administration, patients should rest while the medication takes effect, as nitroglycerin can lower blood pressure, leading to dizziness or fainting if the person stands up too quickly. NITROGLYCERIN MOA Nitroglycerin is a vasodilator primarily used to treat conditions like angina (chest pain), heart failure, and hypertension. It works by relaxing and widening blood vessels, which improves blood flow and reduces the heart’s workload MOA ◦Nitric Oxide (NO) Release ‣ Once administered, nitroglycerin is converted into nitric oxide (NO) within the body. Nitric oxide is a potent vasodilator. ◦Vasodilation ‣ Nitric oxide activates an enzyme called guanylate cyclase inside vascular smooth muscle cells. This enzyme increases the levels of cyclic GMP (cGMP), which in turn causes the smooth muscles to relax. ‣ This relaxation results in vasodilation (widening of blood vessels), particularly in veins, which leads to decreased venous return to the heart (the amount of blood returning to the heart). ◦Decreased Preload ‣ The dilation of veins reduces the preload, or the amount of blood entering the heart. This reduction in preload decreases the heart's workload and oxygen demand. ◦Coronary Artery Dilation ‣ Nitroglycerin also dilates the coronary arteries, which increases blood flow to the heart muscle (myocardium), helping to relieve angina by supplying more oxygen to the heart tissue. ◦Afterload Reduction ‣ At higher doses, nitroglycerin can also dilate arteries, which reduces the afterload (the resistance the heart has to work against when pumping blood out). This further reduces the heart's oxygen demand. NITRO AND PDE5'S It is critical to avoid taking nitroglycerin with PDE5 inhibitors, such as sildenafil (Viagra), tadalafil (Cialis), or vardenafil (Levitra). Combining these medications can lead to a dangerously low drop in blood pressure (hypotension), which can result in serious health complications. DRUG CLASSES USED FOR ANGINA TX Nitrates ◦For acute relief and long-term prevention. Beta-Blockers ◦To decrease heart rate and reduce oxygen demand. Calcium Channel Blockers ◦For vasospastic angina and long-term management. Antiplatelets ◦ To prevent clot formation and reduce the risk of a heart attack. Statins ◦To lower cholesterol and stabilize plaque. Ranolazine ◦ For chronic angina when other treatments are insufficient.  ACE Inhibitors ◦ For patients with comorbidities like hypertension or heart failure. Anticoagulant, Antiplatelet, and Thrombolytic Drugs HEPARIN VS WARFARIN FOR TX OF ACUTE DVT Heparin is preferred for acute treatment of DVT due to its rapid onset of action, which is essential in an acute situation to prevent the clot from growing or spreading. Warfarin is not effective immediately and requires time to take effect (2-3 days), making it unsuitable for immediate anticoagulation in the acute setting, though it is useful for long-term management of DVT. LMW HEPARIN: ENOXAPARIN (WHY IS IT BETTER THAT UNFRACTIONATED) Subcutaneous Administration (Convenient for Outpatient Use): ◦Enoxaparin is typically administered as a subcutaneous injection once or twice a day, which can be done at home or outside the hospital. Preferred Sites: ◦Fatty tissue of the abdomen (about 2 inches away from the belly button) or the thigh. ◦Rotate injection sites to avoid irritation or tissue damage. Injecting: ◦Insert the needle quickly and smoothly into the fatty tissue. ◦Do not aspirate (pull back the plunger). ◦Inject the medication slowly and steadily. ◦Do not rub the injection site after administering to reduce bruising, but gently apply pressure if needed. Dosing and Timing: ◦Dosing: Follow your healthcare provider's instructions for your individual dosage. Doses may vary based on the condition being treated (e.g., DVT, PE) and any other health factors (e.g., renal function). ◦Timing: Administer at the same time each day (if on once-daily dosing) to maintain consistent blood levels. ANTIDOTES Heparin antidote is PROTAMINE SULFATE Warfarin antidote is VITAMIN K ASPIRIN IS NOT A BLOOD THINNER (IT IS A PLATELET AGGREGATION INHIBITOR) APIXABAN DRUG INTERACTIONS Apixaban is an oral anticoagulant used to prevent and treat conditions such as atrial fibrillation, deep vein thrombosis (DVT), and pulmonary embolism (PE). As a direct factor Xa inhibitor, it works by inhibiting the clotting cascade, reducing the risk of blood clot formation. Interactions ◦Anticoagulants and Antiplatelets ‣ Combining apixaban with other blood thinners or antiplatelet medications (e.g., aspirin, clopidogrel, warfarin) increases the risk of serious bleeding. ‣ Avoid combining apixaban with aspirin or other antiplatelet agents unless prescribed by a healthcare provider. ◦Other Anticoagulants ‣ Combining apixaban with heparin or low-molecular-weight heparins (LMWH), such as enoxaparin, can lead to an increased risk of bleeding and is typically contraindicated unless specifically directed by a doctor. ◦Vitamin K  ‣ While vitamin K doesn’t directly affect apixaban like it does with warfarin, foods high in vitamin K (e.g., leafy greens, kale, spinach) are important to maintain consistent intake to avoid any potential interactions. Apixaban’s effect doesn’t fluctuate with vitamin K, unlike warfarin, but sudden large changes in vitamin K intake can affect the balance of coagulation. ◦Herbal Products ‣ Some herbal supplements, such as turmeric, ginger, and garlic, have blood-thinning properties. When combined with apixaban, they may increase the risk of bleeding. It’s important to inform your healthcare provider about all herbal supplements being taken. ◦Alcohol ‣ Excessive alcohol consumption can increase the risk of bleeding and liver damage, which can affect the metabolism of apixaban. It’s advisable to limit alcohol consumption while taking apixaban. Drugs for Deficiency Anemia FOLIC ACID AND B12 Folic acid deficiency and vitamin B12 deficiency both lead to megaloblastic anemia, but their presentations have some important differences. Both cause enlarged red blood cells (megaloblasts) and decreased red blood cell production, but the underlying causes, symptoms, and potential complications differ. Folic Acid Deficiency ◦Caused by: ‣ Dietary deficiency (e.g., poor diet, alcoholism) ‣ Malabsorption (e.g., celiac disease, Crohn’s disease) ‣ Increased demand (e.g., pregnancy, hemolysis, certain medications like methotrexate) ‣ Impaired metabolism (e.g., medications like anticonvulsants or sulfasalazine) Vitamin B12 Deficiency ◦Caused by: ‣ Dietary deficiency (e.g., vegan diet without supplementation) ‣ Pernicious anemia (autoimmune condition that affects intrinsic factor production) ‣ Malabsorption (e.g., celiac disease, Crohn’s disease, gastric surgery, or atrophic gastritis) ‣ Medications (e.g., proton pump inhibitors, metformin, or certain anticonvulsants) ‣ H. pylori infection (can interfere with B12 absorption) PRIORITY TX FOR PT WITH LOW HGB AND HCT When a patient presents with low hemoglobin (Hgb) and hematocrit (Hct), indicating anemia, the priority treatment consideration depends on the underlying cause of the anemia, the severity of symptoms, and the overall clinical picture. Before initiating treatment, it’s crucial to identify the cause of the low Hgb and Hct. The causes of anemia are typically classified into three categories: ◦Blood loss: This can be due to acute or chronic bleeding (e.g., gastrointestinal bleeding, trauma, heavy menstruation, etc.). ◦Decreased red blood cell production: This may be due to nutrient deficiencies (e.g., iron, B12, folate), bone marrow disorders, or chronic kidney disease. ◦Increased red blood cell destruction (hemolysis): This includes conditions like sickle cell anemia, autoimmune hemolytic anemia, or thalassemia. Initiating Tx ◦Stabilize the patient: Focus on oxygenation, fluid balance, and transfusions if necessary for severe anemia. ◦Identify the cause of the anemia with a thorough workup. ◦Treat the underlying cause of the anemia (e.g., iron supplementation, vitamin replacement, blood loss management). ◦Monitor for complications of both anemia and treatments.