Htn and jnc8
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This document discusses the detection, evaluation, and treatment of hypertension. It begins by covering methods for detecting hypertension, including through ambulatory blood pressure monitoring. Next, it addresses recommendations for evaluating patients diagnosed with hypertension. Finally, the document outlines lifestyle modifications and medications that can be used to treat hypertension through therapeutic lifestyle changes and references several studies on sodium and potassium regulation in the kidneys and the use of diuretics and antihypertensive drugs.
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Htn and jnc8
- 1. Detection, Evaluation and Treatment of Hypertension Clinton Pong, MD Tufts/CHA Family Medicine, Fellow October 2014
- 2. DETECTION
- 4. Ambulatory Blood-Pressure Monitor. Pickering TG et al. N Engl J Med 2006;354:2368-2374.
- 5. Pickering TG et al. N Engl J Med 2006;354:2368-2374.
- 6. EVALUATION
- 7. Recommended Evaluation of Patients with Hypertension. Moser M, Setaro JF. N Engl J Med 2006;355:385-392.
- 9. Moser M, Setaro JF. N Engl J Med 2006;355:385-392.
- 10. Moser M, Setaro JF. N Engl J Med 2006;355:385-392.
- 11. Secondary Causes of Resistant Hypertension. Moser M, Setaro JF. N Engl J Med 2006;355:385-392.
- 12. Therapeutic Lifestyle Changes “TLC” and medications TREATMENT
- 13. Lifestyle Modifications to Prevent or Manage Hypertension. August P. N Engl J Med 2003;348:610-617.
- 14. Molecular Mechanisms Implicated in the Retention of Sodium and Loss of Potassium by the Kidneys in Primary Hypertension. Adrogué HJ, Madias NE. N Engl J Med 2007;356:1966-1978.
- 15. Molecular Pathways Implicated in the Generation of Increased Arterial and Arteriolar Smooth- Muscle Tone by an Excess of Sodium and a Deficit of Potassium in Primary Hypertension. Adrogué HJ, Madias NE. N Engl J Med 2007;356:1966-1978.
- 16. Sites of Diuretic Action in the Nephron. Ernst ME, Moser M. N Engl J Med 2009;361:2153- 2164.
- 17. Indications for the Use of Antihypertensive Drugs, Contraindications, and Side Effects. August P. N Engl J Med 2003;348:610-617.
- 19. James, P.A., et al. (2014) 2014 Evidence- Based Guideline for the Management of High Blood Pressure in Adults Report From the Panel Members Appointed to the Eighth Joint National Committee (JNC 8). JAMA. Published online December 18, 2013. doi:10.1001/jama.2013.284427 NHLBI. (2003) JNC7 Reference Card. NIH Publication No. 03-5231 http://www.nhlbi.nih.gov/files/docs/guidelines /phycard.pdf
Hinweis der Redaktion
- Figure 1. Ambulatory Blood-Pressure Monitor. The sphygmomanometer cuff is connected to the monitor by means of a tube that goes under the shirt.
- Figure 2. 24. 24-Hour Blood-Pressure Tracing in a Patient with Hypertension. The white zones indicate the normal ranges of systolic pressure (top) and diastolic pressure (bottom). Adapted from the dabl 24-hour Ambulatory Blood Pressure Measurement reporting system, dabl Disease Management Systems (Ireland) (www.dabl.ie).
- Figure 1. Treatment of Resistant Hypertension. NSAIDs denotes nonsteroidal antiinflammatory drugs.
- Figure 2. Molecular Mechanisms Implicated in the Retention of Sodium and Loss of Potassium by the Kidneys in Primary Hypertension. Solid arrows indicate an increase or stimulation, and the broken arrow indicates inhibition. Numbers on the left denote the approximate percentage of reabsorption of filtered sodium in each nephronal segment during normal conditions. Several influences acting on the luminal sodium transporters and the basolateral sodium pump stimulate sodium retention and potassium loss. Promotion of sodium reabsorption by the activated epithelial sodium channel (ENaC) generates a more negative luminal membrane voltage (Vm) in the collecting duct that enhances potassium secretion through the luminal potassium channel and promotes kaliuresis. NHE-3 denotes sodium–hydrogen exchanger type 3, ACE angiotensin-converting enzyme, NKCC2 sodium–potassium2 chloride cotransporter, and NCC sodium–chloride cotransporter. PST 2238 (rostafuroxin) antagonizes the effect of digitalis-like factor on the sodium pump.
- Figure 3. Molecular Pathways Implicated in the Generation of Increased Arterial and Arteriolar Smooth-Muscle Tone by an Excess of Sodium and a Deficit of Potassium in Primary Hypertension. Solid arrows indicate an increase or stimulation, and broken arrows indicate a decrease or inhibition. The inhibition of the sodium pump and the resulting stimulation of the sodium–calcium exchanger type 1 (NCX1) increase the intracellular concentration of calcium that in turn triggers actin–myosin interaction and stimulation of vascular contraction. Na+ i denotes intracellular sodium concentration, K+ i intracellular potassium concentration, Ca2+ i intracellular calcium concentration, Vm membrane potential, and RyR ryanodine-receptor calcium channel. PST 2238 (rostafuroxin) antagonizes the effect of digitalis-like factor on the sodium pump. SEA-0400 is a specific inhibitor of the bidirectional NCX1 preferentially blocking the calcium influx pathway.
- Figure 1. Sites of Diuretic Action in the Nephron. The percentage of sodium reabsorbed in a given region is indicated in parentheses. “K+-sparing agents” collectively refers to the epithelial sodium-channel inhibitors (e.g., amiloride and triamterene) and mineralocorticoid-receptor antagonists (e.g., spironolactone and eplerenone). Sodium is reabsorbed in the distal tubule and collecting ducts through an aldosterone-sensitive sodium channel and by activation of an ATP-dependent sodium–potassium pump. Through both mechanisms, potassium is secreted into the lumen to preserve electroneutrality. Sodium-channel inhibitors preserve potassium by interfering with the sodium–potassium pump, whereas mineralocorticoid-receptor antagonists spare potassium through their inhibitory effect on aldosterone. NaHCO3 denotes sodium bicarbonate.