Posts Tagged ‘Renal Disease’

Medical Views on Renal Disease – Hypertension

Comments: 0April 30th, 2011 by admin



Monitor your hypertensive patient with renal disease for fluid overload. Assess his fluid status by taking his daily weights, checking his fluid intake and output and breath sounds, and checking him for peripheral edema. Maintain fluid restrictions, as ordered, and assess his serum electrolyte levels for hyperkalemia, hyperphosphatemia, hypocalcemia, and hyponatremia. Administer a calcium-based phosphate binder, as necessary. And restrict has potassium intake, as ordered.

Monitor your patient’s hemoglobin level and hematocrit for anemia. If the physician prescribes erythropoietin for anemia, administer it I. V or subcutaneousiy, as ordered. Because the drug may worsen your patient’s hypertension, monitor his blood pressure closely.

If the physician prescribes an antihypertensive drug, administer it, as ordered. Monitor the drug’s effectiveness by measuring your patient’s blood pressure frequently. For a hospitalized patient, expect to measure it every 4 hours for the first 24 hours. For an outpatient, plan to measure it two or three times a day for the first day or two.

Cautiously administer drugs excreted by the kidneys. Such drugs include digitalis glycosides, aminoglycosides, penicillin, tetracyclines, and narcotics. If the physician has prescribed any of these drugs, he may have to modify your patient’s dosage. Do not administer meperidine to your hypertensive patient with renal disease because its metabolite is cleared by the kidneys and can cause seizures as it accumulates.

Some More Facts

If the physician has prescribed dietary restrictions, help your patient design a diet plan for maintaining the restrictions or refer him to a dietitian, as needed. If the physician has prescribed a fluid restriction, tell your patient to comply with the restriction by calculating his intake and output.

Teach him the name of each prescribed drug and its dosage and therapeutic and adverse effects. If the physician has prescribed a calcium-based phosphate binder, tell your patient not to take iron because aluminum and calcium bind the iron. Tell him to avoid over-the-counter drugs, such as laxatives and antacids, that contain magnesium.

Instruct your patient on self-care measures, such as taking his daily weights and measuring his blood pressure. Teach him to identify edema and electrolyte imbalances, such as hyperkalemia. Tell him to report either of these to his physician.

If your patient will have a home care nurse, tell him that she’ll perform physical assessments, including measuring his daily weights and urine output, checking his breath sounds, and checking for edema. She’ll also assess him for signs and symptoms of electrolyte imbalances and evaluate his compliance with the drug regimen and dietary restrictions.

Tell the patient that she’ll provide assistance as he adapts to his illness and its accompanying restrictions. She may suggest support groups and counseling, if needed. She’ll provide emotional support and encourage him and his family to participate actively in the treatment program.

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Restless Leg Syndrome

Comments: 0June 2nd, 2010 by admin



I have run this mile countless times, not around the neighborhood nor the local track, but simply in my bed each night as I try to fall asleep. The nagging need to move my legs beneath the sheets is overwhelming. I get out of bed. I walk through the house. I try running water over my feet and legs. I hang my legs over the edge of the bed and dangle my feet. Pacing the floor again, I try sleeping on the sofa. I have tried a variety of medications and have avoided certain foods and drinks prior to bed. My symptoms go away for a while. Some nights I simply fall asleep due to exhaustion. This scene repeats itself and to varying degrees of aggravation.

What is this sleep malady and why am I affected by the inability to relax and fall asleep peacefully? I am not alone in this affliction. It is called Restless Leg Syndrome or simply RLS. Approximately 10% of the population is affected. The syndrome is characterized by the urge to move the legs and usually manifests during periods of inactivity and at night prior to falling asleep. Women are affected nearly twice as often as men. Women who are multiparous (who have had more than one child) are primarily affected and the symptoms tend to worsen with subsequent pregnancies.

The syndrome often becomes worse with age and is frequently diagnosed in middle age. RLS often can be a secondary symptom of conditions that cause iron deficiencies. This is perhaps why RLS presents itself during pregnancy when iron deficiencies can occur. End stage renal disease and neuropathies can also cause RLS symptoms. The severity of symptoms range from mild to uncomfortably irritating to painful. Management of RLS, depending on the severity, can involve simple lifestyle changes, such as diet and exercise or in severe cases medications that can be prescribed by a family physician.

Diagnosis usually is based on the subjective information of the recipient. Are the symptoms alleviated by moving the limbs? Is there a family history of RLS? Do certain types of medications help to alleviate or aggravate symptoms? When are symptoms most noticeable? Are there problems with falling asleep and staying asleep? Is there an anemia or an iron deficiency present? Is there an underlying disease present that would cause RLS? The answers to these questions help make the diagnosis.

Often times the victim may present with a normal physical exam. Typically the patient’s main complaint is fatigue and lack of sleep. Their sleep problems are often described as an uncomfortable, creeping, nagging sensation in their legs that does not allow for falling asleep. The feeling is uncomfortable enough to cause the person to “have to” move their legs in order to rid themselves of the sensation. The arms can sometimes be involved as well. The symptoms are alleviated as long as the legs continue to move. Once movement has stopped the uncomfortable sensation begins again. So goes the pattern. The severity varies from night to night and the symptoms may dissipate for several weeks to several months and then return.

The symptoms can also occur during any period of inactivity, whether it is sitting down to read, watch TV, or travel or any time the body is required to sit still. Eighty percent of those affected experience Periodic Limb Movement Disorder or PLMD. This is a jerking motion of the limbs that occur throughout the night and disrupts the sleep cycle. PLMD is different from RLS in that the movements are totally involuntary. The diagnosis of PLMD is made by a sleep study at medical facilities that do sleep monitoring. In either case, the cause of the disorder is not known. It is believed that the chemical neurotransmitter dopamine, which carries information to the nerve cells, is possibly not functioning correctly and therefore an imbalance of this substance contributes to the development of RLS.

Interestingly enough, although it is diagnosed frequently in middle age there are those who are affected early in life. Genetics definitely is a factor in determining early onset of the syndrome. Those with family members affected can have symptoms present as infants. In my particular case, my mother suffers from RLS and my symptoms appeared in my early teens. The fact that I have had four children has made the symptoms even more pronounced. It is estimated that 50% of those with RLS have a genetic predisposition. Others develop RLS as a secondary symptom of other disorders. Again, those with anemia or low iron levels can develop RLS. It is important to have your physician perform a serum ferritin and iron level to determine if iron deficiency exists. Once anemia is corrected the symptoms of RLS are usually alleviated.

Those suffering from kidney failure, diabetes, Parkinson’s disease and peripheral neuropathies often exhibit RLS. Again treating the underlying condition will usually resolve the RLS. Pregnancy is a tremendous contributing factor particularly in the last trimester. Once delivery has occurred the symptoms lessen. However, as mentioned previously multiple pregnancies tend to cause the symptoms to remain. Medications also can be a contributing factor. Antinausea, antipsychotic, and some cold and allergy medications can reek havoc on the RLS sufferer. At one point my sleep was so disrupted that I resorted to nightly sleep aids containing diphenhydramine. Little did I know this was contributing to my RLS. Once I stopped the over the counter sleep aid, my nightly occurrences of the “jimmy legs” stopped as well.

RLS can affect our daily productivity. Lack of concentration, lack of motivation and memory loss are all byproducts of sleep disruption. RLS is often underdiagnosed or misdiagnosed. Common misdiagnoses are depression, insomnia, arthritis, neuropathies and night cramps. Discuss your symptoms with your physician. Identifying a problem is often half the battle. If there is a positive family history, if you experience the urge to move your limbs voluntarily or involuntarily throughout the night and are experiencing sleep interruptions its quite possible that RLS is present. If involuntary, periodic limb movement disorder is suspected, be aware that there are lifestyle changes that can help tremendously.

Pharmacotherapy includes dopaminergic drugs. Levodopa is a first line standard therapy for this disorder. Pergolide (Permax

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Chronic Renal Failure

Comments: 0August 31st, 2009 by admin



Individuals with chronic renal failure and uremia show a constellation of symptoms, signs, and laboratory abnormalities additionally to those observed in acute kidney injury. This reflects the long-standing and progressive nature of their renal impairment and its results on many kinds of tissues.

Thus, osteodystrophy, neuropathy, bilateral little kidneys shown by abdominal ultrasonography, and anemia are typical initial findings that recommend a chronic course for a individual newly diagnosed with renal failing about the basis of elevated BUN and serum creatinine.

One of the most typical cause of continual renal failing is diabetes mellitus, adopted closely by hypertension and glomerulonephritis. Polycystic kidney disease, obstruction, and virus are among the less typical brings about of chronic renal failing. The pathogenesis of acute renal disease is very different from that of continual renal illness.

Whereas acute injury towards the kidney results in death and sloughing of tubular epithelial cells, frequently followed by their regeneration with reestablishment of regular architecture, continual injury results in irreversible loss of nephrons. Being a outcome, a greater practical burden is borne by fewer nephrons, manifested as an improve in glomerular filtration pressure and hyperfiltration.

For factors not nicely understood, this compensatory hyperfiltration, which can be thought of being a form of “hypertension” at the level of the individual nephron, predisposes to fibrosis and scarring (glomerular sclerosis). Being a outcome, the rate of nephron destruction and reduction raises, therefore speeding the progression to uremia, the complicated of symptoms and signs that occurs when residual renal purpose is inadequate.

Owing towards the tremendous practical reserve of the kidneys, up to 50% of nephrons could be lost without any short-term evidence of functional impairment. This is why people with two healthy kidneys are able to donate a single for transplantation. When GFR is further reduced, leaving only about 20% of initial renal capability, some degree of azotemia (elevation of blood vessels levels of products usually excreted by the kidneys) is noticed.

Nevertheless, patients might be largely asymptomatic simply because a new constant state is achieved in which blood vessels levels of those products are not higher sufficient to cause overt toxicity. However, even at this apparently stable level of renal purpose, hyperfiltration-accelerated evolution to end-stage chronic renal failure is in progress.

Furthermore, simply because individuals with this level of GFR have small practical reserve, they can very easily become uremic with any additional tension (eg, virus, obstruction, dehydration, or nephrotoxic medicines) or with any catabolic state connected with increased turnover of nitrogen-containing products with reduction in GFR.

The pathogenesis of continual renal failure derives in part from the mixture from the poisonous results of (1) retained products usually excreted by the kidneys (eg, nitrogen-containing items of protein metabolic process), (2) regular products for example hormones now present in elevated amounts, and (3) lack of normal products of the kidney (eg, loss of erythropoietin).

Excretory failure outcomes also in fluid shifts, with increased intracellular Na+ and drinking water and decreased intracellular K+. These alterations may contribute to subtle alterations in purpose of a host of enzymes, transport systems, and so on. Patients with chronic renal failing typically have some degree of Na+ and water excessive, reflecting loss of the renal route of salt and water excretion.

A moderate degree of Na+ and drinking water excess might happen without having objective indicators of extracellular fluid excessive. However, continued excessive Na+ ingestion contributes to congestive heart failure, hypertension, ascites, peripheral edema, and weight gain. About the other hand, excessive drinking water ingestion contributes to hyponatremia.

A typical recommendation for the patient with continual renal failing is to prevent excessive salt intake and to restrict fluid intake to ensure that it equals urine output plus 500 mL (insensible losses). Further adjustments in amount standing can be made either through using diuretics (in a patient who nevertheless makes urine) or at dialysis.

Because these individuals also have impaired renal salt and water conservation mechanisms, they’re a lot more sensitive than normal to sudden extrarenal Na+ and water losses (eg, vomiting, diarrhea, and increased sweating with fever). Under these circumstances, they a lot more easily create ECF depletion, additional deterioration of renal purpose (which may not be reversible), and even vascular collapse and shock.

The symptoms and indicators of dry mucous membranes, dizziness, syncope, tachycardia, and decreased jugular venous filling suggest progression of amount depletion. Hyperkalemia is a severe problem in chronic renal failing, particularly for individuals whose GFR has fallen under 5 mL/min. Above that level, as GFR falls, aldosterone-mediated K+ transportation in the distal tubule increases inside a compensatory fashion.

Thus, a patient whose GFR is between 50 mL/min and 5 mL/min is dependent on tubular transport to maintain K+ balance. Treatment with K+-sparing diuretics, ACE inhibitors, or -blockers-drugs that may impair aldosterone-mediated K+ transport-can, therefore, precipitate dangerous hyperkalemia in a individual with chronic renal failure.

Individuals with diabetes mellitus (the primary trigger of continual renal failure) may have a syndrome of hyporeninemic hypoaldosteronism. This syndrome is really a situation in which lack of renin manufacturing by the kidney diminishes the levels of angiotensin II and, therefore, impairs aldosterone secretion.

As a outcome, impacted individuals are unable to compensate for falling GFR by enhancing their aldosterone-mediated K+ transportation and, therefore, have relative difficulty handling K+. This difficulty is usually manifested as hyperkalemia even before GFR has fallen under 5 mL/min.

Finally, not only are patients with chronic renal failure a lot more susceptible towards the effects of Na+ or amount overload, but they are also at greater risk of hyperkalemia in the face of sudden loads of K+ from either endogenous sources (eg, hemolysis, virus, trauma) or exogenous sources (eg, stored blood vessels, K+-rich foods, or K+-containing medications).

The diminished capacity to excrete acid and generate base in continual renal failing results in metabolic acidosis. In most instances when the GFR is above 20 mL/min, only reasonable acidosis develops prior to reestablishment of a new constant state of buffer production and usage. The fall in blood vessels pH in these people can usually be corrected with 20-30 mmol (2-3 g) of sodium bicarbonate by mouth every day.

Nevertheless, these individuals are extremely susceptible to acidosis within the event of a sudden acid load or the onset of problems that improve the generated acid load. Several problems of phosphate, Ca2+, and bone metabolic process are noticed in continual renal failing as a result of a complex series of events.

The key factors in the pathogenesis of those problems include (1) diminished absorption of Ca2+ from the gut, (a couple of) overproduction of PTH, (three) disordered vitamin D metabolism, and (4) chronic metabolic acidosis. All of these factors contribute to enhanced bone resorption.

Hypophosphatemia and hypermagnesemia can happen via overuse of phosphate binders and magnesium-containing antacids, even though hyperphosphatemia is more typical. Hyperphosphatemia contributes towards the improvement of hypocalcemia and thus serves as an additional trigger for secondary hyperparathyroidism, elevating blood PTH levels.

The elevated blood vessels PTH additional depletes bone Ca2+ and contributes to osteomalacia of chronic renal failing (see later discussion). Congestive heart failure and pulmonary edema can develop in the context of amount and salt overload.

Hypertension is a typical finding in chronic renal failing, also generally on the basis of fluid and Na+ overload. However, hyperreninemia is also a recognized syndrome in which falling renal perfusion triggers the failing kidney to overproduce renin and thereby elevate systemic blood stress.

Pericarditis resulting from irritation and inflammation from the pericardium by uremic toxins is a complication whose incidence in continual renal failure is decreasing owing to earlier institution of renal dialysis. Increased cardiovascular risk is a complication seen in patients with chronic renal failure and remains the leading trigger of mortality in this population.

It results in myocardial infarction, stroke, and peripheral vascular disease. Cardiovascular risk factors in these patients include hypertension, hyperlipidemia, glucose intolerance, chronic increased cardiac output, and valvular and myocardial calcification being a consequence of increased Ca2+ x PO43 product as nicely as other, less well-characterized factors from the uremic milieu.

Individuals with continual renal failing have marked abnormalities in red blood cell count, white blood vessels cell purpose, and clotting parameters. Normochromic, normocytic anemia, with signs and symptoms of listlessness and simple fatigability and hematocrit levels typically within the range of 20-25%, is a consistent function.

The anemia is due chiefly to lack of production of erythropoietin and lack of its stimulatory effect on erythropoiesis. Thus, individuals with chronic renal failure, regardless of dialysis standing, show a dramatic improvement in hematocrit when treated with erythropoietin (epoetin alpha).

Additional causes of anemia may include bone marrow suppressive effects of uremic poisons, bone marrow fibrosis due to elevated blood vessels PTH, toxic effects of aluminum (from phosphate-binding antacids and dialysis solutions), and hemolysis and blood loss associated to dialysis (while the individual is anticoagulated with heparin).

Individuals with chronic renal failure show abnormal hemostasis manifested as elevated bruising, increased blood vessels reduction at surgery, and an elevated incidence of spontaneous GI and cerebrovascular hemorrhage (including both hemorrhagic strokes and subdural hematomas).

Laboratory abnormalities include prolonged bleeding time, decreased platelet element III, abnormal platelet aggregation and adhesiveness, and impaired prothrombin usage, none of that are totally reversible even in well-dialyzed individuals. Uremia is connected with elevated susceptibility to infections, considered to be because of to leukocyte suppression by uremic toxins.

The suppression appears to become higher for lymphoid cells than neutrophils and seems also to affect chemotaxis, the acute inflammatory response, and delayed hypersensitivity more than other leukocyte functions. Acidosis, hyperglycemia, malnutrition, and hyperosmolality also are considered to contribute to immunosuppression in continual renal failing.

The invasiveness of dialysis and the use of immunosuppressive medicines in renal transplant individuals also contribute to an increased incidence of infections. CNS signs and symptoms and indicators might variety from mild sleep disorders and impairment of mental concentration, lack of memory, errors in judgment, and neuromuscular irritability (manifested as hiccups, cramps, fasciculations, and twitching) to asterixis, myoclonus, stupor, seizures, and coma in end-stage uremia.

Asterixis is manifested as involuntary flapping motions seen when the arms are extended and wrists held back to “stop visitors.” It’s because of to altered nerve conduction in metabolic encephalopathy from the broad range of brings about, including renal failure.

Peripheral neuropathy (sensory higher than motor, lower extremities higher than upper), typified through the restless legs syndrome (poorly localized sense of discomfort and involuntary movements from the lower extremities), is a common discovering in continual renal failing and an important indication for starting dialysis.

Patients receiving hemodialysis can develop aluminum toxicity, characterized by speech dyspraxia (inability to repeat words), myoclonus, dementia, and seizures. Likewise, aggressive acute dialysis can outcome in a disequilibrium syndrome characterized by nausea, vomiting, drowsiness, headache, and seizures inside a individual with really high BUN amounts.

Presumably, this really is an impact of rapid pH or osmolality alter in ECF, resulting in cerebral edema. Nonspecific GI findings in uremic patients include anorexia, hiccups, nausea, vomiting, and diverticulosis. Even though their precise pathogenesis is unclear, many of these findings improve with dialysis. Ladies with uremia have reduced estrogen amounts, which perhaps explains the high incidence of amenorrhea and also the observation that they hardly ever are capable to carry a pregnancy to term.

Regular menses-but not a higher rate of productive pregnancies-typically return with frequent dialysis. Similarly, low testosterone levels, impotence, oligospermia, and germinal cell dysplasia are common findings in males with continual renal failing. Lastly, continual renal failure eliminates the kidney as a website of insulin degradation, thereby increasing the half-life of insulin.

This typically has a stabilizing effect on diabetic patients whose blood glucose was previously hard to control. Skin modifications arise from numerous from the results of continual renal failure currently discussed.

Patients with continual renal failing may show pallor because of anemia, skin color changes related to accumulated pigmented metabolites or even a gray discoloration resulting from transfusion-mediated hemochromatosis, ecchymoses and hematomas being a result of clotting abnormalities, and pruritus and excoriations being a outcome of Ca2+ deposits from secondary hyperparathyroidism. Lastly, when urea concentrations are extremely higher, evaporation of sweat leaves a residue of urea termed “uremic frost.”

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