Ebook Renal physiology (5th edition): Part 2
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Ebook Renal physiology (5th edition): Part 2
REGULATION OF POTASSIUM BALANCEOBJECTIVESupon completion of this chapter, the student should be able to answer the following questions:1I low does the Ebook Renal physiology (5th edition): Part 2e body maintain K homeostasis?2what is the distribution of K’ within the body compartments? Why is this distribution important?3What are the hormones and factors that regulate plasma K* levels?. Why is this regulation important?4How do the various segments of the nephron transport K'. and how does t Ebook Renal physiology (5th edition): Part 2he mechanism ofK' transportby these segments determine how much K* is excreted in the urine?5Why are the distal tubule and collecting duct so importanEbook Renal physiology (5th edition): Part 2
t in regulating K’ excretion?6How do plasma K levels, aldosterone, vasopressin, tubular fluid flow rate, and acid-base balance influence K’ excretion?REGULATION OF POTASSIUM BALANCEOBJECTIVESupon completion of this chapter, the student should be able to answer the following questions:1I low does the Ebook Renal physiology (5th edition): Part 2ein synthesis, growth, enzyme function, resting membrane potential, and cardiac and neuromuscular activity. Despite wide fluctuations in dietary K* intake, I K‘Ị in cells and extracellular fluid (ECF) remains remarkably constant. Two sets of regulatory mechanisms safeguard K* homeostasis. First, sev Ebook Renal physiology (5th edition): Part 2eral mechanisms regulate the IK* ] in the ECF. Second, other mechanisms maintain the amount of K* in the body constant by adjusting renal K* excretionEbook Renal physiology (5th edition): Part 2
to match dietary K* intake. The kidneys regulate K+ excretion.OVERVIEW OF K+ HOMEOSTASISTotal body K' is 30 mEq/kg of body weight, or 3500 mEq for a REGULATION OF POTASSIUM BALANCEOBJECTIVESupon completion of this chapter, the student should be able to answer the following questions:1I low does the Ebook Renal physiology (5th edition): Part 2is required for many cell functions, including cell growth and division and volume regulation. Only 2% of total body K* is located in the ECF, where its normal concentration is approximately 4 mEq/L. IK ’ in the ECP that exceeds 5.0 mEq/L constitutes hyperkalemia. Conversely, IK4 ] in the ECF of les Ebook Renal physiology (5th edition): Part 2s than 3.5 mEq/L constitutes hypokalemia.Hypokalemia is one of the most common electrolyte disorders in clinical practice and can be observed in as115Ebook Renal physiology (5th edition): Part 2
116RENAL PHYSIOLOGYFIGURE 7-1 ■ The effects of variations in plasma K* concentration on the resting membrane potential of skeletal muscle. HyperkalemiREGULATION OF POTASSIUM BALANCEOBJECTIVESupon completion of this chapter, the student should be able to answer the following questions:1I low does the Ebook Renal physiology (5th edition): Part 2e depolarizing phase of the action potential. Hypokalemia hyperpolarizes the membrane potential and thereby reduces excitability because a larger stimulus is required to depolarize the membrane potential to the threshold potential. Resting indicates the “normal” resting membrane potential. Normal th Ebook Renal physiology (5th edition): Part 2reshold indi cates the membrane threshold potential.many as 20% of hospitalized patients, rhe most common causes of hypokalemia include administrationEbook Renal physiology (5th edition): Part 2
of diuretic drugs (see chapter IO), surreptitious vomiting (i.e., bulimia), and severe diarrhea. Gitelman syndrome (a genetic defect in the Na+ Cl- sREGULATION OF POTASSIUM BALANCEOBJECTIVESupon completion of this chapter, the student should be able to answer the following questions:1I low does the Ebook Renal physiology (5th edition): Part 2 disorder and is seen in 1% to 10% of hospitalized patients. Hyperkalemia often is seen in patients with renal tailure, in persons taking drugs such as angiotensin converting enzyme inhibitors and K' sparing diuretics (see Chapter 10), in persons with hyperglycemia (i.e., high blood sugar), and in t Ebook Renal physiology (5th edition): Part 2he elderly. Pseudohyperkalemia, a falsely high plasma 1K‘|, is caused by traumatic lysis of red blood cells while blood is being drawn. Red blood cellEbook Renal physiology (5th edition): Part 2
s, like all cells, contain K', and lysis of red blood cells releases K ‘ into the plasma, artificially elevating the plasma |K'The large concentrationREGULATION OF POTASSIUM BALANCEOBJECTIVESupon completion of this chapter, the student should be able to answer the following questions:1I low does the Ebook Renal physiology (5th edition): Part 2ATPase). This K+ gradient is important in maintaining the potential difference across cell membranes. Thus K+ is criticalfor the excitability of nerve and muscle cells and for the contractility of cardiac, skeletal, and smooth muscle cells (f igure 7-1).IN THE CLINICCardiac arrhythmias arc produced Ebook Renal physiology (5th edition): Part 2by both hypokale mia and hyperkalemia. The electrocardiogram (ECG; Figure 7-2) monitors the electrical activity of the heart and is a quick and easy wEbook Renal physiology (5th edition): Part 2
ay to determine whether changes in plasma |K I influence rhe heart and other excitable cells. In contrast, measurements of the plasma [K*] by the clinREGULATION OF POTASSIUM BALANCEOBJECTIVESupon completion of this chapter, the student should be able to answer the following questions:1I low does the Ebook Renal physiology (5th edition): Part 2 T waves on the ECG. further increases in the plasma [K*] prolong the PR interval, depress the ST segment, and lengthen the QRS interval on the ECG. Finally, as the plasma |K‘| approaches 10 mEq/L, the p wave disappears, rhe QRS interval broadens, the ECG appears as a sine wave, and the ventncles fi Ebook Renal physiology (5th edition): Part 2bnllatc (Í.C., manifest rapid, uncoordinated contractions of muscle fibers). Hypokalemia prolongs the QT interval, inverts the T wave, and lowers theEbook Renal physiology (5th edition): Part 2
ST segment on rhe ECG.REGULATION OF POIZVX5IUIVI DMƯMSUCI I zFIGURE 7-2 Electrocardiograms From persons with varying plasma K’ concentrations. HyperkaREGULATION OF POTASSIUM BALANCEOBJECTIVESupon completion of this chapter, the student should be able to answer the following questions:1I low does the Ebook Renal physiology (5th edition): Part 2icine, cd s, Balli more, J 999, Williams Ớ Wilkins.)After a meal, the K+ absorbed by the gastrointesti nal tract enters the ECF within minutes (Figure 7 3). If the K* ingested during a normal meal (=33 mEq) were to remain in the ECF compartment (1'1 L), the plasma [K* J would increase by a potential Ebook Renal physiology (5th edition): Part 2ly lethal 2.4 mEq/L (33 mEq added to 14 L of ECF):33 mEq/14 I. = 2.4 mEq/L(7-1)This rise in the plasma [K'j is prevented by the rapid uptake (within mEbook Renal physiology (5th edition): Part 2
inutes) of K‘ into cells. Because the excretion of K' by the kidneys after a meal is relatively slow (within hours), the uptake of K* by cells is esseREGULATION OF POTASSIUM BALANCEOBJECTIVESupon completion of this chapter, the student should be able to answer the following questions:1I low does the Ebook Renal physiology (5th edition): Part 2ually be excreted by the kidneys. This process requires about 6 hours.REGULATION OF PLASMA [K+]As illustrated in Figure 7 3 and Box 7 1, several hor mones, including epinephrine, insulin, and aldoste rone, increase K' uptake into skeletal muscle, liver, bone, and red blood cells by stimulating Na' K Ebook Renal physiology (5th edition): Part 2‘-ATPase, the Na* K' 2C1 symporter, and the Na‘-C1 symporter in these cells. Acute stimulation of K‘ uptake (i.e., within minutes) is mediated by an iEbook Renal physiology (5th edition): Part 2
ncreased turnover rate of existing Na'-K'-ATPase, Na'-K*-2('l , and Na*-Cl transporters, whereas the chronic increase in K* uptake (Ĩ.C., within hoursREGULATION OF POTASSIUM BALANCEOBJECTIVESupon completion of this chapter, the student should be able to answer the following questions:1I low does the Ebook Renal physiology (5th edition): Part 2tract stimulates insulin secretion from the pancreas, aldosterone release from the adrenal cortex, and epinephrine secretion from the adrenal medulla. In118 RENAL PHYSIOLOGYFIGURE 7-3 ■ Overview of potassium homeostasis. An increase in plasma insulin, p-adrenergic agonists, or aldosterone stimulates Ebook Renal physiology (5th edition): Part 2 K’ movement into cells and decreases plasma K’ concentration ([K'J), whereas a decrease in the plasma concentration of these hormones moves K* into cEbook Renal physiology (5th edition): Part 2
ells and increases plasma |K'|. a-Adrenergic agonists have the opposite effect. The amount of K' in the body is determined by the kidneys. A person isREGULATION OF POTASSIUM BALANCEOBJECTIVESupon completion of this chapter, the student should be able to answer the following questions:1I low does the Ebook Renal physiology (5th edition): Part 2ulated by plasma [K1], aldosterone, and arginine vasopressin.Urine90-95 mEq of K*/dayREGULATION OF POTASSIUM BALANCEOBJECTIVESupon completion of this chapter, the student should be able to answer the following questions:1I low does theGọi ngay
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