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Cardiovascular and Renal System.docx

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Dalhousie University
NURS 2050
Cynthia Barkhouse Mckeen

CARDIOVASCULAR SYSTEM / RENAL SYSTEM Glomerulus- all small filtrates get filtered (except large proteins like albumin). NaCl is most prevalent. Diuretics work by blocking reabsorption of NaCl ∆ excreting water (prevents the passive reabsorption of water) ∆ increased urine is directly related to NaCl reabsorption it blocks. ∆ Block the most NaCl reabsorption = most profound dieresis. Rationale: since at the end of the tubule, most is reabsorbed, if you catch it earlier, you will block more. Diuretics at the end have the least impact. Greatest impact are the ones that work at the proximal tubule (Osmotic diuretics= rarely used). *** But loop diuretics are the most effective (high ceiling) Drug Excretion: by the kidneys via 1. Glomerular filtration: (all small molecules go through here, no pumps/passive process)  electrolytes, amino acids, drugs, metabolic wastes  large molecules remain in the blood (proteins/lipids)  Nonselective process 2. Active tubular secretion and/or Reabsorption **ACTIVE Processes Reabsorption - proximal convoluted tubule, loop of henle, distal convoluted tubule - most diuretics act to inhibit this process!  Selective process (active transport)  Greater than 99% of the filtrate undergoes reabsorption  Reabsorption is an active process (water is passive) Secretion - proximal convoluted tubule  Selective pumps for organic acids and organic bases  Wastes, drugs, toxins  Can pump drugs from blood to filtrate 3. Passive, flow dependent, diffusion ** Give a drug to inhibit the secretion of another drug. This will allow less drug to be eliminated and the concentration of the drug will be higher in the blood for longer. ∆↑ half life Aldosterone (Retain Na, Excrete K)  Mineralocorticoid of adrenal cortex (estrogens/testosterone, glucocorticoids, mineralocorticoids)  Stimulates Na reabsorption from the distal nephron  Causes a loss of K+ (loss of K because excreted) ADH (anti diuretic hormone) (Retain sodium, Reabsorb water)  Acts @ collecting duct – regulates H2O conservation o Makes it more permeable to H2O o Without ADH the collecting duct is impermeable to H2O  Can affect “concentration” of urine o ADH deficiency – e.g. DI (dilute urine) o ADH excess – e.g. SIADH (concentrated urine) **anti diuretic hormones concentrate urine Diuretics  Treat hypertension (high blood pressure)  Mobilize fluid in edematous states (heart failure, cirrhosis, renal disease)  This class of drug can have numerous indications!! Common mechanism:  Blocking SODIUM and CHLORIDE reabsorption  More solute in the nephron – creates osmotic pressure and prevents the passive reabsortion of water  Most diuretics act on luminal surface of tubular cells Classes: 1. Loop diuretics (high ceiling diuretics)  furosemide (Lasix™) (IV or PO) (thick segment –ascending limb of henle’s loop)  Can keep giving large doses without reaching a peak  Good in those with renal impairment (don’t need ↑GFR) • Ascending loop of Henle • 20% of filtered Na+ & Cl- load = more profound diuresis • Rapid onset • IV for urgent use • Oral* - potential for ↓efficacy in edematous states and in patients with renal dysfunction and uremia. Uses: 1. Edematous states (A = poor) 2. Pulmonary edema 3. HTN Adverse Effects:  Hypotension  Hypokalemia (can be severe)  Hyponatremia  Hypochloremia  Ototoxicity (rare)- IV, rapid infusion, caution with other drugs that cause this effect  Hyperglycemia  Hyperuricemia  Hyperlipidemia  Hypocalcemia (different than thiazides) but not usually significant because Ca+ is actively reabsorbed at the distal convoluted tubule 2. Thiazide diuretics (low ceiling diuretics)  Hydrochlorothiazide (early distal convoluted tubule)  Maximal effects occur at low doses (Clinically this means that titrating the dose above a certain point will not provide more diuresis)  Caution in those with allergy to sulfonamides  Not good in those with renal impairment. Need ↑GFR to work!!  Can be found in combination products • Commonly with ACE-I (angiotensin converting enzyme inhibitor) Uses: 1. Hypertension (**drug of choice. Many can be tx with this alone) 2. Edematous states – mild to moderate edema Mechanism:  ↑excretion of Na+, CL-, K+ and H2O (blocks R of NaCl/Water E K)  By blocking reabsorption Na+ & Cl- in the early segment of the distal convoluted tubule (10% of filtered Na load) Adverse Effects:  Hypokalemia – most common cause  Hypercalcemia (not usually  Dehydration (uncommon) significant, in contrast to loops which causes hypoglycemia)  Hyperglycemia (diabetics)  Ottotoxicity – not a factor, can be  Hyperuricemia (↑gout, ↑uric acid) combined with ottotoxic drugs  Hyponatremia  Hypomagnesemia 3. Potassium sparing diuretic AKA Aldosterone antagonists (Gets rid of Na, retains K)  spironolactone (late distal convoluted tubule/collecting duct)  can cause synthesis of Na+/K+ pumps  Aldosterone normally: • increases reabsorption of Na+ and H2O along with the excretion of K+ in the distal tubules •Is the main Na+ retaining hormone from adrenal gland Uses: 1. Hypertension edematous states (delayed, minor diuresis)  Delay in onset of effect - due to time required to synthesize Na+/K+ transporters  Diuresis – minimal because filtered Na+ load remaining 2. Severe heart failure Adverse Effects:  Hyponatremia  Hyperkalemia  Endocrine Effects- because of its steroid like structure. The body mistakes it for other hormones. (Gynecomastia, menstral irregularities, hirsutism, deepened voice) 4. Osmotic diuretics (Proximal tubule) & carbonic anhydrase inhibitors (used less often) Diuretics – Adverse Effects Grouped 1. Hypovolemia – decreased blood volume 2. Acid base imbalance 3. Electrolyte imbalances Cardio/Renal II **RAAS (renin-angiotensin-aldosterone system) help regulate blood pressure blood volume, fluid & electrolyte balance Promotes- Remodeling, Cardiac fibrosis and myocyte death Angiotension Converting Enzyme (ACE inhibitors) – renal elimination • Many: captopril, enalapril, quinapril, ramipril • Reduces preload and afterload Uses: • Congestive heart failure (CHF) • Hypertension • Post MI (reduces mortality following an MI) • Nephropathy (slows progression of renal disease) Adverse Effects 1. First dose hypotension (titrate slowly especially in those with overactive RAAS), caused by widespread vasodilation) 2. Cough (5-10% or more) 3. Angioedema (life threatening) 4. Hyperkalemia (especially in those with K+ sparing diuretics or supplements (need to monitor this!) Caused by inhibition of aldosterone release 5. Increase in serum creatinine 6. Fetal injury (pregnancy category x) 7. Renal impairment  CI for those with bilateral renal artery stenosis  Caution for those with renal impairment  In those with severe impairment, consult nephrology Decreased Renal Perfusion Angiotensin II Receptor Blockers - The ―sartans‖ or ―ARBs‖ • Blocks receptors for angiotensin II and therefore the actions of angiotensin II E.g. valsartan, candesartan, losartan • Similar pharmacologic effects as ACE Inhibitors • Similar side effect- Potentially less cough as does not lead to increased production of bradykinin RAAS Digoxin  Used for “inotropic” properties in CHF  May decrease hospitalizations and improve exercise tolerance  Problems with toxicity  Controversy regarding use in certain populations (has a narrow therapeutic index)  Inotropic agent- Inhibits Na+-K+-ATPase: o This causes increase in intracellular Ca2+ o Increase myocardial contractility  “Parasympathomimetic”: o Increases vagal impulses and increases response of SA node to acetylcholine o Result = decrease automaticity of SA node and conduction through AV node  Has a long half life  Monitor serum level if suspected toxicity, changes to drug regimen, changes in renal fx Mechanism of Action: Inhibiting the Na+/K+ ATPase promotes calcium accumulation myocytes which prevents myocytes from restoring proper ionic composition following an action potential Adverse Effects 1. Dysrrhythmia  Hypokalemia (caution with non K+sparing diuretics!)  Potassium competes with digoxin for binding to Na+/K+ ATPase- decreased K+ increases dig induced inhibition of the pump 2. Digoxin levels  Narrow therapeutic index- Toxicity can occur within the therapeutic range  Toxicity – if suspected, good to do a digoxin
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