Disorders of fluid volume: .

Because Na is the major osmotical y active ion in the ECF, total body Na content determines ECF volume. Deficiencyor excess of total body Na content causes ECF volume depletion or overload. Serum Na concentration does notnecessarily reflect total body Na.
Dietary intake and renal excretion regulate total body Na content. When total Na content and ECF volume are low, thekidneys increase Na conservation. When total Na content and ECF volume are high, Na excretion (natriuresis)increases so that volume decreases.
Renal Na excretion can be adjusted widely to match Na intake. Renal Na excretion requires delivery of Na to thekidney and so depends on renal blood flow and GFR. Thus, inadequate Na excretion may be secondary to decreasedrenal blood flow, as in renal disease or heart failure.
The renin-angiotensin-aldosterone axis is the main regulatory mechanism of renal Na excretion. In volume-depletedstates, GFR and Na delivery to the distal nephron decrease, causing release of renin. Renin cleaves angiotensinogen(renin substrate) to form angiotensin I. ACE then cleaves angiotensin I to angiotensin II. Angiotensin II increases Naretention by decreasing the filtered load of Na and enhancing proximal tubular Na reabsorption. Angiotensin II alsostimulates the adrenal cortex to secrete aldosterone, which increases Na reabsorption via multiple renal mechanisms.
Angiotensin I can also be transformed to angiotensin III, which stimulates aldosterone release as much as angiotensinII but has much less pressor activity. Aldosterone release is also stimulated by hyperkalemia. Several natriureticfactors have been identified, including atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and a C-typenatriuretic peptide (CNP).
ANP, in cardiac atrial tissue, increases in response to ECF volume overload (eg, heart failure, renal disease, cirrhosiswith ascites) and primary aldosteronism and in some patients with essential hypertension. Decreases have occurred insome patients with nephrotic syndrome and presumed ECF volume contraction. High levels increase Na excretion andincrease GFR even if BP is low.
BNP is synthesized mainly in the atria and left ventricle and has similar triggers and effects to ANP. BNP assays areavailable, and high BNP level is used to diagnose volume overload. CNP, in contrast to ANP and BNP, is primarilyvasodilatory.
Na depletion requires inadequate Na intake plus abnormal losses from the skin, GI tract, or kidney (defective renal Naconservation). Defective renal Na conservation may be caused by primary renal disease, adrenal insufficiency, ordiuretic therapy. Na overload requires higher Na intake than excretion; however, because normal kidneys can excretelarge amounts of Na, Na overload generally reflects defective renal Na excretion.
EXTRACELLULAR FLUID VOLUME CONTRACTION
ECF volume contraction is a decrease in ECF volume caused by loss of water and total body Na content. Causesinclude vomiting, sweating, diarrhea, burns, diuretic use, and renal failure. Clinical features include diminished skinturgor, dry mucous membranes, tachycardia, and orthostatic hypotension. Diagnosis is clinical. Treatment involvesadministration of Na and water. A decrease in ECF (ECF volume contraction [hypovolemia]) is not the same as a decrease in effective plasma volume.
Decreased effective plasma volume may occur with decreased ECF, but it may also occur with an increased ECF (eg,in heart failure, hypoalbuminemia, capil ary leak syndrome).
ECF volume contraction usually involves loss of Na; Na loss always causes water loss. Depending on many factors,plasma Na concentration can be high, low, or normal despite the decreased total body Na content. Common causes ofECF volume depletion are listed in Table 1: Fluid and Electrolyte Metabolism: Common Causes of Extracellular FluidVolume Depletion Symptoms and Signs
ECF volume depletion is suspected in patients with a history ofinadequate fluid intake (especial y in comatose or disoriented Common Causes of Extracellular Fluid
patients); increased fluid losses; diuretic therapy; and renal or Volume Depletion
In mild (5%) ECF volume depletion, the only sign may bediminished skin turgor. The patient may complain of thirst. Dry Extrarenal
mucous membranes do not always correlate with volume depletion, especial y in the elderly or in mouth-breathers.
Oliguria is typical. When ECF volume has diminished by 5 to Dialysis: Hemodialysis, peritoneal dialysis 10%, orthostatic tachycardia, hypotension, or both are GI: Vomiting, diarrhea, nasogastric suction generally present, although orthostatic changes can occur inpatients without ECF volume depletion, particularly those Skin: Excessive sweating, burns, exfoliation deconditioned or bedridden. Skin turgor (best assessed at theupper torso) may be decreased. If dehydration exceeds 10%, signs of shock can occur (eg, tachypnea, tachycardia,hypotension, confusion, poor capil ary refil ).
Renal/adrenal
Diagnosis
Acute renal failure: Diuretic phase of recovery Diagnosis is usually clinical. If the cause is obvious and easily Adrenal disease: Addison's disease (glucocorticoid correctible (eg, acute gastroenteritis in an otherwise healthy patient), laboratory testing is unnecessary; otherwise, serumelectrolytes, BUN, and creatinine are measured. Plasma osmolality and urine Na, creatinine, and osmolality are Diabetes mellitus with ketoacidosis or extreme measured if there is suspicion of clinically meaningful electrolyte abnormality that is not clear from serum tests and for patients with cardiac or renal disease. Invasive monitoringis necessary for patients with previously unstable heart failure Salt-wasting renal disease (medullary cystic disease, interstitial nephritis, some cases of Central venous pressure and pulmonary artery occlusionpressure are decreased in ECF volume depletion, butmeasurement is rarely required.
During ECF volume depletion, normal y functioning kidneys conserve Na. Thus, the urine Na concentration is usually <15 mEq/L; the fractional excretion of Na (urine Na/serum Na divided by urine creatinine/serum creatinine) is usually <1%; also, urine osmolality is often > 450 mOsm/kg. If metabolic alkalosis is combined with ECF volume depletion, urineNa concentration may be high; in this instance, a urine Cl concentration of < 10 mEq/L more reliably indicates ECFvolume depletion. Misleadingly high urinary Na (generally > 20 mEq/L) or low urine osmolality can also occur due torenal Na losses resulting from renal disease, diuretics, or adrenal insufficiency. ECF volume depletion frequentlyincreases the BUN and plasma creatinine levels with the ratio of BUN to creatinine often > 20:1. Values such as Hctoften increase in volume depletion but are difficult to interpret unless baseline values are known.
Treatment
The cause of volume depletion is corrected and fluids are given to replace existing volume deficits as wel as any
ongoing fluid losses and to provide daily fluid requirements. Mild-to-moderate volume deficits may be replaced by
increased oral intake of Na and water if the patient is conscious and is not vomiting severely. When volume deficits
are severe or when oral hydration is impractical, IV 0.9% saline is given. Typical IV regimens are presented discussed
in Shock and Fluid Resuscitation: Intravenous Fluid Resuscitation; oral regimens, discussed in Dehydration and Fluid
Therapy: Oral Rehydration.
EXTRACELLULAR FLUID VOLUME EXPANSION
ECF volume expansion is caused by an increase in total body Na content. It typically occurs in heart failure,nephrotic syndrome, and cirrhosis. Clinical features include weight gain, edema, and orthopnea. Diagnosis isclinical. Treatment aims to correct volume expansion and its cause. An increase in total body Na is the key pathophysiologic event. It increases osmolality, which triggers compensatorymechanisms that produce water retention.
Movement of fluid between interstitial and intravascular spaces depends on Starling's forces at the capil aries.
Increased capil ary hydrostatic pressure, as occurs in heart failure; decreased plasma oncotic pressure, as occurs innephrotic syndrome; or a combination, as occurs in severe cirrhosis, shifts fluid into the interstitial space, producingedema. In these conditions, subsequent intravascular volume depletion increases renal Na retention, which maintainsfluid overload. Common causes of volume overload are listed in Table 2: Fluid and Electrolyte Metabolism: PrincipalCauses of Extracellular Fluid Volume Overload Symptoms and Signs
Weight gain and weakness may occur before edemaformation. Dyspnea on exertion, decreased exercise tolerance, Principal Causes of Extracellular Fluid
tachypnea, orthopnea, and paroxysmal nocturnal dyspnea can Volume Overload
also occur early when volume overload is caused by left Renal Na retention
ventricular dysfunction. Elevated jugular venous pressure mayproduce jugular venous distention.
Early symptoms of edema may include puffy eyes on rising inthe morning and tight shoes at the end of the day. Edema is often dependent in heart failure. In ambulatory patients, edemais in the feet and lower legs; patients at bed rest develop edema on the buttocks, genitals, and posterior thighs; women who lie on only one side may develop edema in the dependent breast.
Edema can be accompanied by myriad findings, including pulmonary rales, elevated central venous pressure, an S3gallop, and an enlarged heart with pulmonary edema and/or Renal disease, especial y nephrotic syndrome pleural effusions on chest x-ray. In cirrhosis, edema isfrequently confined to the lower extremities and accompanied Decreased plasma oncotic pressure
by ascites. Other signs of cirrhosis include spider angiomas, gynecomastia, palmar erythema, and testicular atrophy. Innephrotic syndrome, edema is often diffuse, occasionally with generalized anasarca, pleural effusions, and ascites;periorbital edema occurs frequently, but not invariably.
Reduced albumin synthesis (liver disease, Diagnosis
Increased capillary permeability
Symptoms and signs, including dependent edema, are usuallydiagnostic. Physical findings may suggest a cause. For instance, edema plus ascites suggests cirrhosis. Rales and S3 suggest heart failure. Generally, diagnostic testing includesserum electrolytes, BUN, creatinine, and any other tests directed at the cause (eg, chest x-ray for suspected heart failure). Causes of isolated lower extremity swelling (eg,lymphedema, venous stasis, venous obstruction, local trauma) Treatment
Iatrogenic
In patients with heart failure, maximizing left ventricular function(eg, by using inotropic agents or afterload reduction) can Administration of excess Na (eg, 0.9% normal increase Na delivery to the kidneys and Na excretion.
Treatment of the causes of nephrotic syndrome depends onthe specific renal histopathology.
e inhibit Na reabsorption in the ascending limb of the loop of Henle. Thiazide diuretics inhibit Na reabsorption in the distal tubule. Both loop diuretics and thiazide diuretics increase excretion of Naand thus water. K wasting can be problematic in some patients; K-sparing diuretics, such as amilorid , one inhibit Na reabsorption in the distal nephron and col ecting duct. When used alone, they increase Na excretion, but only modestly. Both triamter e been combined with a thiazide to prevent K Many patients respond insufficiently to diuretics; common contributing factors include inadequate treatment of thecause of volume overload, noncompliance with dietary Na restriction, hypovolemia, and renal disease. Diuresis canfrequently be achieved by increasing the dose of a loop diuretic or combining it with a thiazide.
After correction of volume overload, maintenance of euvolemia may require restriction of dietary Na unless theunderlying condition can be eliminated. Diets containing 3 to 4 g/day Na are generally adequate, are fairly weltolerated, and work reasonably wel in mild-to-moderate volume overload diets for heart failure. Advanced cirrhosis andnephrotic syndrome often require more severe Na restriction (≤ 1 g/day). K salts are often substituted for Na salts tomake Na restriction tolerable; however, care should be taken, especial y in patients receiving K-sparing diuretics orACE inhibitors and in those with renal disease, because potential y fatal hyperkalemia can result.
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