Renal Medications PDF

Renal Medications Tonicity Intravenous solutions Isotonic: osmotic pressure remains the same ○ 0.9% NaCl (normal saline), LR (lactated ringers), D5W Similar concentration of solutes like blood plasma Hypotonic: lower osmotic pressure ○ 0.45% NaCl, D5W (Dextrose 5% in water...

Renal Medications Tonicity Intravenous solutions Isotonic: osmotic pressure remains the same ○ 0.9% NaCl (normal saline), LR (lactated ringers), D5W Similar concentration of solutes like blood plasma Hypotonic: lower osmotic pressure ○ 0.45% NaCl, D5W (Dextrose 5% in water) Causes fluid to move out of the veins into surrounding tissues Hypertonic: higher osmotic pressure ○ 3% NaCl, D10W (Dextrose 10% in water), D5NS, D5L Causes fluid to move into veins from surrounding tissues Crystalloids Mechanism of Action Solutions contain fluid and electrolytes normally found in the body. They do not contain proteins colloid no risk for viral transmission, anaphylaxis or alteration in coax better for treating dehydration rather than expanding plasma volume used as maintenance fluids to compensate for insensible fluid losses replaced fluid fluids manage specific fluid and electrolyte disturbances and promote urinary flow. Types of Crystalloids NS 0.9% Lactated ringers Dextrose 3.3% dextrose and 0.3% NS D5W and 0.225% NS (D51/4NS) Plasma-lyte 0.45% NaCl 3% NaCl D5W and 0.45% NS Colloids Mechanism of Action Specifically albumin natural protein that is normally produced in the liver responsible for generating approximately 70% of colloid oncotic pressure, sterile solution of serum albumin that is prepared from pooled blood, plasma, serum or placenta obtained from healthy donors pasteurized to destroy any contaminants Blood Products Only class of fluids that carries oxygen increases tissue oxygenation increases plasma volume, and most expensive and least available fluid Increase colloid oncotic pressure and plasma volume Packed RBC Used to increase oxygen carrying capacity and patients with anaemia, very low haemoglobin or who have lost up to 25% of their total blood volume Whole Blood Whole blood is more beneficial in cases of extreme loss of blood volume because whole blood contains plasma plasma proteins, help draw fluid back into vessels from surrounding tissues Potassium Mechanism of Action Most abundant positively charged electrolyte inside of cells makes up 95% of body’s Potassium is an intracellular potassium content outside the cells range from 3.5 to 5 mmol per litre potassium levels are critical to normal body function that includes ○ muscle contraction ○ transmission of nerve impulses ○ regulation of heartbeat ○ maintenance of acid base ○ balance, and isotonicity Diuretic Drugs Mechanism of Action Diuretics act at different sites along the nephron, the functional unit of the kidney, where they interfere with sodium and water reabsorption. The nephron consists of several segments, each with a unique function: 1. Proximal Convoluted Tubule (PCT): Responsible for the bulk of sodium, chloride, and water reabsorption. 2. Loop of Henle: Divided into the descending limb (permeable to water) and the ascending limb (impermeable to water but actively transports Na+, K+, and Cl-). 3. Distal Convoluted Tubule (DCT): Involved in further sodium reabsorption and regulation of potassium and calcium. 4. Collecting Duct: The final site of sodium and water reabsorption, influenced by aldosterone and antidiuretic hormone (ADH). Thiazide Diuretics Hydrochlorothiazide, Chlorthalidone, Indapamide Site of Action: Distal Convoluted Tubule (DCT) Mechanism: Thiazide diuretics primarily inhibit the Na+/Cl- symporter (also called the sodium-chloride cotransporter) in the distal convoluted tubule. This prevents sodium (and chloride) from being reabsorbed back into the blood. As a result, more sodium and water are excreted in the urine. Effects: ○ Increased sodium, chloride, and water excretion.  ○ Potassium loss (hypokalemia) due to compensatory effects in the distal nephron. ○ Calcium retention (can be beneficial in conditions like osteoporosis). Uses: Thiazides are commonly used for: ○ Hypertension (first-line treatment). ○ Heart failure (especially for mild edema). ○ Kidney stones (due to calcium-sparing effect). Loop Diuretics Furosemide, Bumetanide, Torsemide Site of Action: Thick Ascending Limb of the Loop of Henle Mechanism: Loop diuretics inhibit the Na+/K+/2Cl- symporter in the thick ascending limb of the loop of Henle. This transporter is responsible for reabsorbing sodium, potassium, and chloride. By blocking this transporter, loop diuretics cause a significant reduction in sodium and water reabsorption. Effects: Profound diuresis (increased urine output). Potassium loss (hypokalemia), magnesium loss (hypomagnesemia), and calcium loss (hypocalcemia). Increased renal blood flow by causing venodilation and decreasing preload, which is beneficial in conditions like heart failure. Uses: Heart failure (especially for severe edema and pulmonary edema).  Acute kidney failure. Hypertension (especially in resistant cases). Hypercalcemia (due to its ability to increase calcium excretion). Potassium Sparing Diuretics Examples: Spironolactone, Eplerenone, Amiloride, Triamterene Site of Action: Collecting Duct (Spironolactone and Eplerenone act on aldosterone receptors, while Amiloride and Triamterene inhibit sodium channels) Mechanism: Aldosterone Antagonists (Spironolactone, Eplerenone): These drugs block the action of aldosterone, a hormone that increases sodium reabsorption in the collecting duct. By antagonizing aldosterone, these drugs reduce sodium retention and water reabsorption while sparing potassium. Sodium Channel Blockers (Amiloride, Triamterene): These drugs directly block sodium channels in the collecting duct, preventing sodium reabsorption and thus promoting diuresis. They are called "potassium-sparing" because they do not promote potassium excretion like other diuretics do. Effects: Mild diuresis compared to loop and thiazide diuretics. Potassium retention (hyperkalemia), which is a significant side effect, especially when used with other diuretics or in patients with renal dysfunction. Uses:  Heart failure (particularly for patients with hyperaldosteronism). Edema due to cirrhosis or nephrotic syndrome. Hypertension (especially when used in combination with thiazide or loop diuretics to prevent potassium loss). Carbonic Anhydrase Inhibitors Examples: Acetazolamide, Methazolamide Site of Action: Proximal Convoluted Tubule (PCT) Mechanism: Carbonic anhydrase inhibitors work by inhibiting the enzyme carbonic anhydrase in the proximal convoluted tubule. This enzyme normally catalyzes the conversion of carbon dioxide and water into carbonic acid, which dissociates into bicarbonate (HCO₃⁻) and hydrogen ions (H⁺). By inhibiting carbonic anhydrase, these drugs reduce the reabsorption of bicarbonate, sodium, and water, leading to increased urinary excretion of these substances. Effects: Increased excretion of bicarbonate, sodium, potassium, and water. Metabolic acidosis due to bicarbonate loss. Uses: Glaucoma (to reduce intraocular pressure). Altitude sickness (to reduce symptoms of acute mountain sickness by correcting respiratory alkalosis). Epilepsy (occasionally, as an adjunctive treatment). Osmotic Diuretics Examples: Mannitol, Glycerin Site of Action: Proximal Convoluted Tubule and Loop of Henle Mechanism: Osmotic diuretics increase the osmolarity of the filtrate in the nephron, which prevents water reabsorption and leads to increased urine output. Osmotic agents are filtered by the glomerulus but are not reabsorbed, thus creating an osmotic gradient that pulls water into the urine. Effects: ○ Increased urine volume. ○ Reduction in cerebral edema (by drawing fluid out of brain tissue) and intraocular pressure (helpful in conditions like glaucoma). Uses: ○ Cerebral edema (acute situations like traumatic brain injury). ○ Acute renal failure. ○ Increased intraocular pressure (glaucoma). Antihypertensive Drugs Antihypertensive drugs are medications used to lower blood pressure (BP) in individuals with hypertension. These drugs act through various mechanisms to either reduce cardiac output, decrease systemic vascular resistance (SVR), or both. They may target the heart, blood vessels, kidneys, or the nervous system to exert their effects. Adrenergic drugs ACE inhibitors  Angiotensin II receptor blockers (ARBS) Calcium channel blockers Diuretics Vasodilators Direct renin inhibitors Diuretics Mechanism of Action: Diuretics lower blood pressure by reducing blood volume through enhanced excretion of sodium and water in the urine. The reduction in blood volume decreases cardiac output and preload (the amount of blood returning to the heart), which in turn lowers blood pressure. Angiotensin Converting Enzyme (ACE inhibitor) Mechanism of Action: ACE inhibitors block the enzyme angiotensin-converting enzyme (ACE), which converts angiotensin I to angiotensin II, a potent vasoconstrictor. By inhibiting this enzyme: Decreased levels of angiotensin II result in vasodilation, reducing systemic vascular resistance (SVR). Decreased aldosterone secretion lowers sodium and water retention, leading to a reduction in blood volume and preload. Examples: Enalapril, Lisinopril, Ramipril, Captopril Common effects: Dry cough (due to increased bradykinin), hyperkalemia, dizziness, fatigue. Angiotensin II Receptor Blockers (ARBs) Mechanism of Action: ARBs block the angiotensin II type 1 (AT1) receptor, preventing the vasoconstrictor and aldosterone-secreting effects of angiotensin II. Unlike ACE inhibitors, ARBs do not increase bradykinin levels, thus avoiding the cough and angioedema associated with ACE inhibitors. Examples: Losartan, Valsartan, Olmesartan Common effects: Dizziness, hyperkalemia, hypotension, less common cough than ACE inhibitors. Calcium Channel Blockers Mechanism of Action: CCBs inhibit the entry of calcium ions into vascular smooth muscle cells and cardiac muscle cells via L-type calcium channels. This leads to: Vasodilation of the arteries, which reduces systemic vascular resistance (SVR) and lowers blood pressure. In the heart, calcium channel blockers reduce heart rate (especially non-dihydropyridine CCBs), contractility, and conduction velocity in the atrioventricular (AV) node, decreasing cardiac output. Dihydropyridines (e.g., Amlodipine, Nifedipine): ○ Primarily vasodilators, used for hypertension and angina. Non-dihydropyridines (e.g., Verapamil, Diltiazem): ○ Act on both the heart and blood vessels, reducing heart rate, contractility, and conduction, and are used for hypertension and arrhythmias (especially atrial fibrillation).  Common effects: Peripheral edema (especially with dihydropyridines), constipation (especially with verapamil), dizziness, headache. Beta Blockers Mechanism of Action: Beta blockers block beta-adrenergic receptors (β1 and β2) in the heart, kidneys, and vascular smooth muscle. This results in: Decreased heart rate (negative chronotropy), reduced myocardial contractility (negative inotropy), and lowered cardiac output, all of which contribute to lower blood pressure. Beta blockers also reduce renin secretion from the kidneys, which decreases the activity of the renin-angiotensin-aldosterone system (RAAS), leading to vasodilation and reduced blood volume. Examples: Atenolol, Metoprolol, Propranolol, Carvedilol (non-selective) Common effects: Bradycardia, fatigue, depression, erectile dysfunction, bronchospasm (non-selective blockers). Alpha-1 Adrenergic Blockers Mechanism of Action: Alpha-1 blockers selectively block alpha-1 adrenergic receptors in vascular smooth muscle, preventing vasoconstriction by endogenous catecholamines (e.g., norepinephrine). This leads to vasodilation and reduced SVR. Examples: Prazosin, Doxazosin, Terazosin  Common effects: Orthostatic hypotension (especially with the first dose), dizziness, headache, reflex tachycardia. Alpha-2 Agonists Mechanism of Action: Alpha-2 agonists stimulate alpha-2 adrenergic receptors in the central nervous system (CNS), leading to a decrease in sympathetic outflow. This results in: Reduced release of norepinephrine, leading to vasodilation and decreased heart rate. Reduced cardiac output and reduced SVR. Examples: Clonidine, Methyldopa Common effects: Sedation, dry mouth, dizziness, rebound hypertension if discontinued abruptly. Direct Vasodilators Mechanism of Action: Direct vasodilators act directly on the smooth muscle of blood vessels to cause relaxation and vasodilation, which decreases SVR and lowers blood pressure. Hydralazine: Primarily affects arterial dilation. Minoxidil: More potent than hydralazine, can also induce hypertrichosis (excessive hair growth). Examples: Hydralazine, Minoxidil, Nitroprusside Common effects: Reflex tachycardia, fluid retention (may require diuretic use), dizziness, headache. Renin Inhibitors Mechanism of Action: Renin inhibitors block the activity of renin, the enzyme responsible for converting angiotensinogen to angiotensin I, thus preventing the formation of angiotensin II. This leads to vasodilation, decreased aldosterone secretion, and reduced blood volume. Example: Aliskiren Common effects: Hyperkalemia, hypotension, diarrhea, headache.