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BIOD 331 Module 8 /Guaranteed A+ Score
Guide
Module 8: The Renal System 8.1: Structure and Function of the Kidney ● Kidneys filter ¼ of average person’s cardiac output. Process essential ions, reabsorb substances which maintain normal body fluids, excrete waste products through urine, regulate blood pressure and volume, and stimulate RBC production. Vital for maintaining homeostasis ● Adult kidney is bean-shaped, about the size of a fist, weighs approx 5 oz. R kidney lies slightly lower than the L because of the liver’s location just above it. Both kidneys are mostly protected by the rib cage bc of their locations between the T and L3 vertebrae. Kidney’s medial surface is known as the hilus. Hilus is a concave cleft, where ureters, blood vessels, and nerves enter kidney. Kidney is encapsulated in an external fibrous capsule and surrounded by fatty connective tissue. Fatty tissue provides protection from injury & aids to hold the kidney in place. The kidneys are considered retroperitoneal organs meaning they are situated posterior to the peritoneal cavity ● Nephron is the basic structural & functional unit of a kidney. Approx 1 million nephrons in each kidney, function to control concentration of water & soluble materials by filtering the blood, reabsorbing needed materials and excreting waste products as urine. Nephron eliminates wastes from the body, regulates blood volume, pH and pressure, and controls the levels of electrolytes. Each nephron consists of 2 parts, the glomerular capsule (renal corpuscle) and renal tubule. These structures are connected through the tubule to the associated collecting ducts. The glomerular capsule filters the blood while the renal tubule reabsorbs needed materials, and the collecting ducts carry the remaining material away as urine to be excreted ● ‘]
● On longitudinal section, the kidney can be divided into the outer cortex and inner medulla. The outer cortex houses the glomeruli and convoluted tubules (proximal and distal) of the nephron as well as blood vessels. The inner medulla is comprised of the Loop of Henle and cone-shaped masses known as the renal pyramids. Portions of the cortex known as cortical columns project through the medulla to the renal pyramids. Each pyramid forms a lobe of the kidney. The renal pelvis is located at
the centermost region of the kidney. It constitutes a funnel-shaped tube that connects to the ureter as it leaves the hilus. Several extensions of the pelvis called calyces collect urine which drain continuously into the renal pelvis & subsequently into the ureter, which transports the urine to the bladder to be stored ● Nephron Structure and Function ○ Functional unit of the kidney, blood filtration & reabsorption take place. Nephrons can be divided into 1 of 2 groups, cortical nephrons and juxtamedullary nephrons. Cortical nephrons make up 85% of all nephrons. They originate superficially in the cortex & have shorter loops of henle that extend only a short distance into the medulla. Juxtamedullary nephrons make up remaining 15% of all nephrons. They originate deeper in the cortex, and their loops of Henle are thinner and extend into the medulla entirely ○ Nephrons receive their blood supply from 2 systems known as the glomerulus and peritubular capillary network. The glomerulus is a unique system in that it is located between 2 arterioles, afferent and efferent. Arterioles are high resistance vessels resulting in an extremely high-pressure system which can easily force fluid and solutes out of the blood and into the glomerular capillary along its entire length. The peritubular capillaries are low-pressure vessels better suited for reabsorption as opposed to filtration. These capillaries surround the tubules in their entirety allowing rapid movement of solutes and water. Efferent arterioles located deep in the renal cortex turn into long, thin-walled vessels known as the vasa recta. The vasa recta run parallel to the loops of Henle in the medullary region and assist in the exchange of solutes and water flowing in and out of the kidney ○ The glomerulus is composed of a compact mass of capillaries surrounded by a thin, double walled capsule known as the Bowman capsule. Blood flows through the afferent arteriole into the glomerular capillaries, and flows out of the glomerular capillaries into the efferent arteriole. This then leads to the peritubular capillaries. Solutes and fluids are filtered from the blood through the capillary membrane into a fluid-filled space within Bowman capsule. This space is referred to as Bowman space. The blood that is filtered into Bowman space is referred to as filtrate. The mass of capillaries (glomerulus) surrounded by its epithelial capsule (Bowman capsule) that opens into a tubule is collectively referred to as the renal corpuscle ○ The glomerular capillary membrane contains 3 layers: the capillary endothelial layer, the basement membrane, and the single-celled capsular epithelial
3 processes must take place: filtration, reabsorption, and secretion. Filtration takes place in the renal corpuscle while reabsorption and secretion occur in the renal tubules ○ Filtration takes place in the glomerulus across the very porous membrane that lies between the capillaries and the interior of Bowman’s capsule. The filtration that takes place here is referred to as mechanical filtration as it does not require energy. The fluids & solutes such as water, glucose, amino acids, and nitrogenous wastes are forced through the membrane by the high hydrostatic blood pressure that exists in the capillary bed. The capillary pores prevent passage of blood cells and most blood proteins across the membrane. The loss of water from the blood plasma is prevented by retaining the plasma proteins in the capillaries since they maintain the osmotic pressure of the glomerular blood ○ A normal glomerular filtration rate (GFR) is 120-125 ml/min or 180 L/day. Such a rate is possible due to the large surface area of the glomerular capillaries, the large degree of membrane permeability, and the moderate net filtration pressure. The GFR is increased by an increase in the arterial and glomerular blood pressure in the kidneys, and is decreased by a rise in glomerular osmotic pressure most often caused by dehydration. Maintenance of a relatively constant GFR is important for adequate reabsorption of water and other needed nutrients from the filtrate. If the flow of the filtrate is too rapid, needed substances cannot be adequately reabsorbed. If the flow is too slow nearly all of it is reabsorbed, including waste products that would typically be excreted ○ 3 mechanisms that regulate renal blood flow & thereby regulate the GFR despite changes in arterial blood flow: renal autoregulation, nervous system control, and hormonal control ■ Renal autoregulation: Under normal conditions, the GFR is controlled by regulating the diameter of the afferent and efferent arterioles, thereby allowing the kidney to determine its own rate of blood flow. Constriction of the efferent arteriole leads to an increased resistance to outflow from the glomeruli w a subsequent increase in glomerular pressure and the GFR. Constriction of the afferent arteriole causes a reduction in renal blood flow, glomerular pressure, and the GFR. Through this autoregulatory system, kidney can maintain
a constant GFR despite variations in the arterial blood pressure of the rest of the body ■ Nervous system: kidneys are richly innervated by the sympathetic nervous system. Sympathetic activity diverts blood to the heart, brain, and skeletal muscles. Renal autoregulatory system may be superseded by nervous system control. In this event, narrowing of the afferent arteriole is caused by sympathetic nerve fibers followed by release of epinephrine from the adrenal medulla which leads to subsequent decrease in renal flow and the GFR ■ Hormonal control: renin-angiotensin-aldosterone system. RAA system responds when the body’s bp drops too low. Angiotensinogen is a pre- enzyme produced by the liver that is freely circulating in the blood. When bp drops, the enzyme renin is released by the juxtaglomerular JG cells of the nephron. Renin causes constriction of the afferent and efferent arterioles and converts angiotensinogen to angiotensin I. IN the lungs, angiotensin I is converted to angiotensin II. Angiotensin II increases vasoconstriction which increases peripheral blood pressure. Once circulating angiotensin II reached the adrenal cortex, it causes the release of aldosterone which increases reabsorption of sodium and water from the filtrate ○ From Bowman’s capsule, the glomerular filtrate is transported to the tubular portions of the nephron. As it moves through the tubule, needed solutes and fluids are reabsorbed into the peritubular capillaries from the tubular fluid and waste products are secreted from the peritubular capillaries into the tubular fluid. ○ Tubular reabsorption occurs as needed substances move through membrane barriers of the tubule segments to reach the peritubular capillaries. Reabsorption of water & ions are hormonally regulated & may occur through passive or active processes. The greatest amount of tubular reabsorption occurs in the proximal convoluted tubule (PCT). Glucose and amino acids are almost completely reabsorbed in the PCT in addition to water and other ions. Sodium, chloride, potassium, and bicarbonate are 65-80% reabsorbed from the filtrate. ○ From the PCT, the filtrate will move into the loop of Henle. PCT reabsorbs Na and water in equal proportions, loop of Henle reabsorbs more Na and Cl than water. The thinner descending limb of the loop of Henle is highly permeable
deposition of calcium in the bone. Vitamin D occurs in 2 forms, cholecalciferol (taken in through the skin via UV rays from the sun) and ergocalciferol (synthetic vitamin D). Both forms of vitamin D must be chemically activated. The inactive forms of vitamin D will be converted to 25 - hydroxycholecalciferol in the liver and to 1,25-dihydroxycholecalciferol in the kidneys 8.2: Renal Calculi & Glomerulonephritis ● Most common cause of upper urinary tract obstructions are renal calculi (kidney stones). Stones composed of polycrystalline compounds formed from materials that would typically be excreted by the kidneys. The formation of stones is multifactorial. Levels of stone components in the blood and urine, anatomical changes of the urinary tract structures, metabolic and endocrine function, dietary and intestinal absorption, as well as past history of UTIs must all be taken into consideration when determining cause of formation. Risk for stone formation is directly correlated to supersaturated urine. The higher the saturation of stone components (calcium salts, uric acid, magnesium ammonium phosphate, and cystine) in urine, the higher risk for stone development. Stone formation also requires a nucleus made of larger ion clusters that attract smaller crystals or stone components to it. Crystals would break apart on their own as the bonds that hold them together are weak, however the nucleus has stronger attractive forces holding them together forming a stone ● 4 types of kidney stones: calcium stones (oxalate or phosphate), magnesium ammonium phosphate stones, uric acid stones, and cystine stones. Approx 75-80% of kidney stones are calcium stones. They are typically a result of increased concentrations of calcium in blood & urine. Can occur secondary to increased bone resorption, typically associated w immobility, bone disease, or hyperparathyroidism ● Magnesium ammonium phosphate stones form in urine that is alkaline (pH>7). This increase in pH is the result of a UTI caused by bacteria possessing urease. Urease breaks urea into ammonia & CO2. The ammonia will form an ammonium ion which increases urine pH. The resulting stones increase in size as levels of bacteria rise. Account for approx 15% of kidney stones ● Uric acid stones typically coincide w gout. Form when the pH of urine is more acidic. Not visible on x-ray films, account for approx 7% of kidney stones
● Cystine stones are rare, 1-3% of all kidney stones. Most common cause of stones in children. Result of cystinuria which occurs when there is a decrease in tubular absorption of cystine, and is a result of a genetic defect in renal transport ● Hallmark symptom is pain. 2 types of pain depending on location. Renal colic pain is “colicky” pain brought on by stretching of collecting ducts or ureter. This pain occurs as stones 1-5 mm in diameter move through ureter and block flow. Acute, sharp pain that comes in waves, felt in the upper lateral quadrant of the abdomen and the back of the affected side. Termed flank pain. Can radiate to the lower abdominal region, bladder area, perineum, or scrotum. Can be accompanied by clammy, cool skin as well as nausea and vomiting. Non-colicky pain caused by stones that distend the renal pelvis or renal calyces. Can be described as a deep, dull ache in the flank area. Varies in intensity from mild to severe ● Dx and Tx ○ Pts who experience kidney stones often arrive to the hospital w acute flank pain. Dx made based on symptomatology as well as dx testing. Tests may include urinalysis, x-rays, CT scan, intravenous pyelography (IVP), and abdominal u/s. A urinalysis will look at urine pH level, the presence of stone forming crystals, infection, and/or hematuria. As discussed earlier, most stones will appear readily on x-ray film, except for uric acid stones. Non- contrast spinal CT scan is most often used for dx. IVP uses a contract medium that is injected intravenously. This medium will filter through glomeruli allowing the provider to visualize flow through the collecting ducts and ureters. Abdominal u/s is another imaging technique used to identify stones and is often the means for visualization when smaller stones go undetected through other dx methods ○ Tx involves pain management as well as abx therapy if there is a UTI. Most kidney stones that are 5 mm or less will pass on their own. Once a stone has passed, goal for tx is prevention of future stones. Preventative measures often require investigating the initial cause of the stone through urinalysis and blood work. Underlying disease processes should be tx, and lifestyle changes should be encouraged such as increased fluid (water) intake and a decrease in foods that contribute to the synthesis of stone forming elements ○ When a stone cannot pass on its own, removal may be necessary. Ureteroscopic removal is done under fluoroscopic guidance. A small probe is inserted into the urethra, into the bladder, and then into the ureter. The
days after a strep infection. The primary strep infection typically involves the pharynx but may involve the skin. Oliguria (decreased urine output < mL a day) will develop as the GFR decreases. This is one of the first symptoms and is quickly accompanied by proteinuria (protein in urine) and hematuria. Secondary to increased glomerular capillary wall permeability. The RBCs break down in the urine leading to dark brown color. Sodium and water will be retained leading to edema particularly in hands and face, and HTN ○ Lab results will include elevated antistreptococcal antibody (ASO) titer, a decline in serum concentrations of C3 and other complement cascade components, as well as cryoglobulins in the serum. Tx of this type of glomerulonephritis includes elimination of causative infection. Prognosis is very good w tx, and rarely causes chronic kidney disease ○ Chronic glomerulonephritis represents the chronic phase of specific types of glomerulonephritis. Acute can be completely cured w use of abx, however other forms of acute may not resolve and will continue to progress into the chronic phase. Pts w chronic glomerulonephritis often go long periods of little to no symptoms. In most cases, develops insidiously and will slowly progress to chronic kidney disease over years. 8.3: Acute Renal Failure & Chronic Kidney Disease ● Acute Renal Failure ○ Condition in which kidneys fail to filter metabolic waste products from the blood, regulate fluid and electrolyte balance, and control the pH of the extracellular fluids. Can occur as acute or chronic disorder. Acute comes on suddenly & can be reversed if detected early & treated properly. Chronic renal failure occurs as result of irreversible damage to the kidney, developing over the course of years. Approx 26 million American adults suffer from a form of kidney disease ○ Causes of acute can be prerenal, postrenal, or intrarenal ■ Prerenal: most common, hallmark is decreased renal blood flow. If cause of reduction in blood flow is identified quickly, condition can be reversed. Causes include a profuse decrease in blood volume (hemorrhage), impaired perfusion secondary to heart failure, and decreased vascular filling due to anaphylaxis or sepsis. Under normal conditions the kidneys receive 20-25% of the cardiac output. This
large amount of blood supply is necessary for the glomeruli to filter metabolic waste products and balance fluids and electrolytes. A healthy kidney is capable of functioning even w a large reduction in blood flow before damage occurs. Prerenal failure is characterized by a drastic decrease in urine output accompanied by a disproportionate increase of blood urea nitrogen (BUN) in comparison to serum creatine levels. A decrease in renal blood flow leads to a decrease in the GFR. When this occurs, there is a resultant decrease in urine output. An early sign of prerenal failure is a rapid decline in urine output. BUN levels are also affected by the GFR. A lower GFR allows smaller particles such as urea to be reabsorbed back into the blood. Creatinine is a larger particle and is unable to be diffused. Because of this, it will remain in the tubular fluid and the total amount that is filtered is excreted in the urine. End result is elevated ratio of BUN to serum creatinine. Normal ratio is 10:1, in prerenal failure it can elevate to 15:1-20:1 or greater ■ (^) Postrenal: occurs when the outflow of urine from the kidney is impeded. Obstructions can occur throughout the urinary tract-in the ureter (renal calculi), bladder (tumor or neurogenic bladder), or urethra (enlarged prostate). Increase in urine retention causes pressure to build in tubules and nephrons leading to damage. Prostatic hyperplasia is most common cause. Tx involves addressing cause of obstruction so that normal urine flow can resume before permanent damage to nephrons is done ■ (^) Intrarenal: more commonly known as acute kidney injury. Caused by conditions that damage structures within the kidney, namely the glomeruli, vessels, tubules, or interstitium. Major causes include ischemia that accompanies prerenal failure, obstruction, and damage to the tubular structures. Injury to tubules within nephron is the most common of causes and is typically ischemic or toxic in nature ○ Acute tubular necrosis is characterized by the destruction of the tubule epithelial cells accompanied by a sudden decline in renal function. Ischemic acute tubular necrosis (ATN) occurs most frequently among pts who have had major surgery and/or have suffered trauma or burns. Damage to the tissue releases toxins that make tubular cells more susceptible to ischemic effects. Nephrotoxic ATN is brought on by exposure to drugs and other
classify CKD into 5 stages which range from kidney names w normal or elevated GFR, to CKD, and kidney failure. Ultimate goal of staging is implementation of appropriate tx measures to keep pts from progressing into kidney failure ○ ○ Dx when there is kidney damage and/or a GFR < 60 mL/min/1.73m^2 for 3 months or longer. Multiple conditions can cause CKD as they lead to an overall loss of nephrons including HTN, DM, and SLE. Manifests w decrease in number of functioning nephrons and decrease in GFR. GFR is considered best measure of kidney function. Rate at which nephrons are destroyed varies among individuals. For some, decine can occur over months, while may take several years for others. Kidneys have incredible compensatory capability, sings & symptoms do not appear until disease is advanced. Remaining nephrons compensate leading to hypertrophy as they filter more blood and solutes. When compensatory nephrons are destroyed, clinical manifestations begin to appear ○ Clinical presentation will vary & can be very complex as kidneys play such a vital role in homeostasis. Complications include water & electrolyte imbalances, skeletal disorders, anemia, GI disorders, immune dysfunction, and neurologic complications ○
Tx ■ (^) Conservative tx measures are employed to slow rate or prevent nephron destruction. Include UTI management and bp control w non- nephrotoxic drugs, as well as lifestyle changes such as smoking cessation. Measures are utilized in conjunction w tx for underlying cause ■ (^) Dialysis or renal replacement therapy is indicated when advanced uremia or severe electrolyte imbalances occur. While transplantation is preferred tx for advanced CKD, it may not be an option depending on the pt’s health status, comorbidities, and/or donor availability. Dialysis plays a life sustaining role as pts wait for transplantation ■ (^) 2 types of dialysis, hemodialysis and peritoneal dialysis ■ (^) Hemodialysis utilizes an “artificial kidney” to filter blood. Composed of 3 parts, a blood delivery system, dialyzer, and dialysis fluid delivery system. Blood circulates through hollow dialyzer composed of bundles of capillary tubes. Dialysate moves on the outside of tubes. Walls of capillary tubes are composed of semipermeable material which allows all molecules except blood cells & plasma proteins to move in both directions. Waste products will diffuse into the
Specific dietary restriction include a reduction in protein intake. As the metabolism of protein forms nitrogenous waste products, consuming high amounts of protein will increase BUN levels. A decrease in dietary protein will lead to a decrease in BUN levels and and ultimately symptom reduction. If protein intake is reduced, it is important for pts to consume adequate calories in the form of carbohydrates and healthy fats to meet their energy needs. Fluid and electrolyte restrictions depend upon the pt, and the kidney’s ability to excrete sodium and water. Fluid intake greater than the amount the kidney can excrete will result in edema, water intoxication, and circulatory overload. Inadequate hydration will cause hypotension and will further decrease the GFR. If the GFR falls to dangerously low levels during dialysis treatment, dietary potassium must be restricted to prevent serious cardiac events 8.4: Fluid and Electrolyte Balance ● The kidneys are essential for regulating the volume & composition of bodily fluids. This is achieved through the regulation and balance of water and electrolytes. In order to maintain proper water balance, the amount of water taken in each day must equal the amount of water output in a given day ● Water intake and output are closely regulated by the hypothalamic thirst mechanism and antidiuretic hormone (ADH) which is stored in and secreted by the posterior pituitary. ADH, also known as vasopressin, acts on the collecting tubule to increase water absorption. ADH inhibits urine output by increasing number of water channels in cell membrane of collecting ducts. These channels allow water to pass easily from the filtrate and move into the surrounding interstitial space, eventually returning to blood circulation. The release of ADH is connected to the degree of body hydration, allowing the body to respond to dehydration. Many factors cause dehydration such as sweating, vomiting, and diarrhea. ADH will also respond in more life-threatening circumstances such as severe hemorrhage. Blood loss will lead to dangerous drop in bp. The subsequent release of ADH will act to retain up to 99% of water in filtrate. Kidneys will excrete a very small volume of highly concentrated urine. When ADH is not being released, diluted urine is excreted ● Kidneys also regulate osmolarity-amount of solute per unit of volume. Achieved by balancing the reabsorption and secretion of sodium w water
● Aldosterone is secreted by adrenal cortex in adrenal glands under control of RAA system. Upregulates several types of ion channels inside the cells of collecting ducts, such as sodium-hydrogen ion channels. Aldosterone increases Na reabsorption through excretion of H+ ions. Na ions are pumped out of filtrate, H ions are pumped inside then excreted. Water follows salt, Na reabsorption causes water reabsorption. Aldosterone will also increase K secretion through Na/K pumps. Na is pumped out of filtrate to be returned to blood while K is excreted in urine. Main action of aldosterone is to increase blood volume and BP when deeded. Release can occur directly in response to high K levels or low Na levels in extracellular compartment. Normal triggers for RAA system are from the CNS, decreased renal filtrate, decreased osmotic pressure, or decreased bp. Aldosterone control system is slow acting, requiring hours to days to take effect ● Diuretics are substances that act on nephron to increase urinary output. As most diuretic drugs decrease Na reabsorption, less water is reabsorbed from filtrate. Caffeine is a diuretic that causees renal tubules to increase in diameter, increasing amount of flow through tubules. Alcohol is also considered a diuretic as it inhibits release of ADH. Other diuretics act on different parts of the nephron to cause a greater flow of urine. When filtrate moves at a faster rate through the nephron, it allows less time for ions to be removed from the filtrate ● Cardiovascular baroreceptors also act on nephron to regulate blood volume. They are located in the aortic arch and carotid sinus arteries, and are under control of vagus and glossopharyngeal cranial nerves. They are mechanoreceptors, detect stretch inside vessels. The cranial nerves relay information to the medulla, which monitors blood volume in order to maintain normal bp. Blood volume is directly influenced by the Na ion concentration. If blood volume and bp rise, baroreceptors inhibit sympathetic nervous signals to the kidney, causing afferent arterioles that carry blood to the glomerulus to dilate. This increase in size causes a dramatic increase in filtration rate which increases output of water and Na, which reduces blood volume and quickly normalizes pressure ● Fluid and Electrolyte Imbalances ○ Water imbalances include dehydration, over hydration (water intoxication) and edema. Dehydration occurs when water output significantly exceeds water intake. Dehydration can be the result of extreme blood loss, severe burns, DM, diabetes insipidus, long periods of diarrhea or vomiting, and extreme sweating. Symptoms of dehydration include decreased urination, disorientation, dry reddened skin, fever, thickened mucus, thirst, and weight loss. When dehydration occurs, water is first lost from the plasma and
adrenal disease and decreased aldosterone levels. Hypervolemic hypotonic hyponatremia occurs when hyponatremia is accompanied by edema. Occurs w conditions such as heart failure, liver disease, and renal disease. Euvolemic hypotonic hyponatremia occurs when there is a retention of water w a dilution of Na+ while ECF volume remains at normal levels. This occurs when ADH levels are higher than normal causing the body to retain water. This is common during post-operative periods ○ Clinical Presention ■ Acute or chronic depending on severity of sodium dilution. Causes an increase in intracellular water levels because of abnormal flow. Early signs include muscle cramps, weakness, and fatigue. Nausea, vomiting, abdominal cramping, and diarrhea may develop. The nervous system can be severely affected by the increase in intracellular fluid. Lethargy and headache can quickly progress to disorientation, confusion, and gross motor weakness. If sodium levels drop dangerously low, seizures and coma can result. ○ Dx and Tx ■ Dx of hyponatremia require blood work and urinalysis to determine sodium concentration within the body. Tx focuses on underlying cause. If cause is water intoxication, limiting fluids and possibly changing medications that contribute to the condition may be enough. The administration of saline solution (orally or intravenously) may be indicated if the underlying cause is a sodium deficiency ● Hypernatremia ○ Occurs when plasma Na+ levels rise above 145 mEq/L with a serum osmolality greater than 295 mOsm/kg. It is characterized by a deficit of water in relation to the body’s Na+ stores. It can be caused by net water loss or sodium gain. Typically follows a loss of bodily fluids that contain a decreased concentration of Na+, an example being diarrhea. Under normal circumstances, water deficits will stimulate thirst increasing water intake. Hypernatremia can accompany hypodipsia (impaired thirst). This is common among children and the elderly when they cannot express their need to drink ○ Clinical Presentation ■ Clinical SS are result of water loss w thirst being earliest sign. Additional SS include a decrease in urine output, a rise in body temp, and the skin becoming flushed. Mucous membranes will dry out causing a decrease in salivation and tear production. Swallowing will become difficult. If the nervous system becomes affected, agitation, headaches and restlessness occur. Seizures and coma may develop ○ Dx and Tx
■ Dx is made based on physical exam findings indicative of dehydration & blood work. Tx includes treating the underlying cause and replenishing fluids orally or intravenously ● Hypokalemia ○ Occurs when plasma K+ levels fall below 3.5 mEq/L ○ Cause can be inadequate intake, excessive GI, renal, or skin losses, and redistribution between the ICF and ECF compartment ■ Inadequate intake is a common cause. One should take in at least 40- 50 mEq/day through the diet or by supplement. Older adults are at risk for this type as well as people w eating disorders and people on fad diets which restrict certain food groups ■ The kidneys do not have compensatory mechanisms needed to conserve K+ during periods of excessive loss. 80-90% of K+ loss occurs through the urine w remainder being excreted through stool and sweat. A deficit can develop quickly if intake is insufficient. Diuretic therapy (except for K+ sparing diuretics) is the most common cause of hypokalemia ■ Conditions that cause a shift of K+ from the ECF to the ICF compartment will cause a decrease in plasma K+ levels. Insulin therapy increases movement of glucose and K+ into cells. Hypokalemia is common in the tx of diabetic ketoacidosis ○ Clinical Presentation ■ Manifest through multiple system malfunction. GI symptoms can manifest secondary to the atony of intestinal smooth muscle. They include nausea, vomiting, constipation, and abdominal distention. Most serious effects occur when the cardiovascular system is affected. Postural hypotension, bradycardia, and ectopic ventricular arrhythmias may result ○ Dx and Tx ■ Tx is to increase dietary intake of potassium, may also be given intravenously if rapid replacement is necessary ● Hyperkalemia ○ Occurs when plasma K+ levels rise above 5 mEq/L. Rarely occurs in otherwise healthy individuals as body is extremely effective in prevention of K+ accumulation in the ECF. Cause is decreased renal function, excessively rapid administration, or movement of K+ from the ICF to the ECF compartment ■ Most common cause is decreased renal function. Renal failure is almost always accompanied by hyperkalemia
