Chapter 8 - Disorders Of Fluid, Electrolyte, And Acid - Base Balance Flashcards
(39 cards)
What is the composition and compartmental Distribution of Body Fluids?
The intracellular fluid ICF compartment - which consists of the fluid contained contained within all the trillions of cells in the body, contains about two thirds of the body water in healthy adults. It contains almost no Ca; small amounts of Na, Cl, bicarbonate, and PO4; moderate amounts of Mg and large amounts of K.
The extra cellular fluid ECF compartment - is the remaining one third which contains all the fluids outside the cells, including those in the interstitial or tissue spaces and the plasma in the blood vessels. It contains large amounts of Na+, Cl-, moderate amount of bicarbonate, but only small quantities of K+, Mg, Ca, and PO4.
What is the movement of body fluids and electrolytes between compartments? What is tonicity?
The lipid bilateral and transport proteins serve as the primary barriers to the movement of substances across the cell member and that separates the ECF and ICF.
- Dissociation of electrolytes - Electrolytes are substances that dissociate in solution to form charged particles, or ions. NaCl molecule dissociates to form a + Na and - Cl. Particles that do not dissociate into ions are no electrolytes. Positively charged ions are cations and negatively are anion. Ions found in body fluid carry one or two charges. Positive always carries a negative anion. Both ICF and ECF contain equal amounts of anions and cations
- Osmosis and tonicity - the total concentration gradient is the same in both comparative td because of osmotic movement of water. Osmosis refers to the movement of water across a semipermeable membrane. Water diffuses down its concentration gradient, moving form the side of the membrane with a greater concentration of water and lesser concentration of solute particles to the side with a less concentration of solute particles. Osmotic pressure is as water moves across the semipermeable membrane, it generates a pressure. The magnitude of the osmotic pressure represents the hydrostatic pressure needed to oppose. It’s measure by osmole so its either Osmolarity - refers to the osmolar concentration or osmolality - to the osmolar concentration in 1 kit of water. Serum osmolality is largely determined by Na+ and its attendant anions Cl and HCO3 275-295 H2O. Blood urea nitrogen BUN and glucose, both osmotically active, usually account for less the 5%.
Tonicity refers to the tension or effect that a solution with impermeable solutes exerts on cell size because of water movement across the cell membrane. 3 types Isotonic - which has the same effective osmolality of the ICF neither shrink or swell., hypotonic- has lower osmolality they swell, hypertonic - greater osmolality they will shrink.
What is compartmental distribution of body fluids? What are the ECF subdivisions?
Body water - 60% about of the body weight, is distributed between the ICF and ECF. ICF 40% and ECF 20%.
The ECF compartment is further divided into two major subdivisions; the plasma compartment which constitutes 5% of body wight and interstitial compartment 14% of body weight. - acts as a transport vehicle for gases, nutrients, wastes, and other material that move between the vascular compartment and body cells. It also provides a reservoir from which vascular volume can be maintained during periods of hemorrhage or loss of vascular volume. Interstitial gel is a sponge like material supported by collagen fibers, fills the spaces and aids in even distribution of fluid. It is firmer consistency than water, opposes the outflow of water from the capillaries, preventing the accumulation of free water in the interstitial spaces. A third minor subdivision is the transcellular compartment it includes cerebrospinal fluid and fluid contained in the various body spaces such as the peritoneal, pleural and pericardial cavities and joint spaces. Only 1% of ECF
What is capillary/interstitial fluid exchange? What are the 4 main forces?
The transfer of water between the vascular and interstitial compartments occurs at the capillary level.
.1 the capillary filtration pressure - which pushes water out of the capillary into the interstitial spaces, uses hydrostatic pressure - since this pressure results from the weight of water. It is usually 30-40 mm Hg at the arterial end and 10-15 mm Hg at the venous end, and 25mm Hg in the middle. It increases 1 mm Hg pressure for every 13.6 mm of distance from the heart.
2. The capillary colloidal osmotic pressure - which pulls water back into the capillary - abut 28 mm Hg is the osmotic pressure generated by the plasma proteins that are too large to pass through the pores of the capillary wall
- The interstitial or tissue hydrostatic pressure - which opposes the movement of water out of the capillary. Which is normally negative, contributes to the outward movement of water into the interstitial spaces.
- The interstitial colloidal osmotic pressure. - which pulls water out of the capillary into the interstitial spaces. Which reflects the small amount of plasma protein that normally escape into the interstitial spaces from the capillary, also pulls water out of the capillary into the tissue spaces.
Normally, the combination of these four forces is such that only a small excess of fluid remains in the interstitial compartment. This excess fluid is removed from the interstitial by the lymphatic system and returned to the systemic circulation. It removes the plasma proteins and osmotically active particulate master from the tissue spaces.
What is edema? What are the physiologic mechanisms that contribute to edema formation.
Can be defined as palpable swelling produced by an increase in interstitial fluid volume.
1. Increase the capillary filtration pressure, Increased vascular volume, venous obstruction, liver disease with portal vein obstruction, acute pulmonary edema. 2. Decrease the capillary colloidal osmotic pressure.- increased loss of plasma proteins, decreased production of plasma proteins (liver disease, malnutrition), 3. Increase capillary permeability - inflammation, allergic reactions, malignancy, tissue injury and burns 4. Produce obstruction to lymph flow. Malignant obstruction of lymphatic structures, surgical removal of lymph nodes.
Manifestations - the effects of edema are determined largely by its location. Edema of the brain, larynx, and lungs are acute, life threatening conditions. Non may interfere with movement, limiting joint motion. This tissue is more susceptible to injury and ischemia tissue damage (pressure ulcers), can shut off blood flow, can be disfiguring, causing psychological effects and disturbances. Pitting edema occurs when the accumulation of interstitial fluid exceeds the absorptive capacity of the tissue gel. The tissue water becomes mobile and can be translocated with pressure from a finger. No pitting is which the swollen area becomes firm and discoloured, occurs when plasma proteins have accumulated in the tissue spaces and coagulated. Seen mostly in areas of localized infection or trauma.
Assessment and treatment - Methods for assessing edema include daily weight, visual assessment, measurement of the affected part, appplication of finger pressure to assess for pitting edema. Pitting is on a scale of +1 to 4. Lymphedema Is hard to diagnose. CT or MRI assist. Treatment of edema is usually directed toward maintaining life when the swelling involves vital structures, correcting or controlling the cause, and preventing tissue injury. Can be as elevating the feet. Diuretic therapy. Serum albumin levels can be measured and albumin given if needed. Elastic support stocking and sleeves inc interstitial fluid pressure and resistance to outward movement. Usually with conditions of venou or lymphatic obstruction
What is third space accumulation?
It represents the loss or movement and trapping of ECF in a transcompartmental space. The serous cavities are part of the transcompartmental compartment located in strategic body areas where there is continual movement of body structures - pericardial sac, the peritoneal cavity, and the pleural cavity. The serous cavities, which are closely linked with lymphatic drainage syste, use the same mechanisms for interstitial fluid exchange as other areas of the body. The milking action of the moving structures, such as the lungs, continually forces fluid and plasma proteins back into lymphatic channels, healing to keep theses cavities empty. Hydro may be used to indicated the presence of excessive fluid in one of the serous cavities such as hydro thorax referring to fluid in the pleural cavity. Peritoneal cavity as ascitis, serous cavities is effusion.
What is the water and sodium balance? What’s the regulation of water balance?
The distribution of body fluids between the ICF and ECF compartments relies on the concentration of ECF water and sodium. Water provides approximately 90-95% of the volume of body fluids and sodium salt approximately 90-95% fo ECF solutes, Positive water balance results in a dec in body fluid osmolality and ECF sodium concentration due to diluting effects of the excess water.
TBW total body water account for a large % of body weight. Men 60% young Older 52%. Women 50% dec to 46% in elderly. Obesity dec TBW to as low as 30-40%. Infants normally have more TBW than older children or adults 75%. MAin source of water gain is through oral intake and metabolic processes. The largest loss of water occurs through the kidney The urine output thwart is required to eliminate these wastes is called obligatory urine output. Water loses that occur through evaporative losses from skin to moisten the air in the respiratory system are referred to as insensible water losses because they occur without a person’s awareness.
What is regulation of sodium balance?
Sodium is the most plentiful electrolyte in the ECF compartment, with a concentration ranging from 135-145 mEq/L. Sodium does not readily cross the cell membrane; as a result, only a small amount is located in the ICF compartment. As the major cation in the ECF compartment, Na+ and its attendant Cl-and HCO3- anions account for approximately 90-95% of the osmotic activity in the ECF. Thus, serum osmolality usually varies with changes in serum sodium concentration. It’s normally ingested through the GI tract. Although many of our foods have much more then needed, we only need as little as 500 mg/day to meet requirements. Most sodium losses occur through the kidney. When sodium intake is limited or conservation of sodium is needed, the kidneys are able to reabsorb almost all the Na+ that has been filtered in the glomerulus. Sodium leaves the skin by way of sweat glands, which secrete a hypotonic solution containing both sodium and chloride.
What are the two mechanisms of water and sodium regulation?
The physiologic mechanisms for regulating body levels of water; thirst, which is primarily a regulator of water intake, and the anti diuretic hormone ADH, which controls the output of water by the kidney. They function in the maintenance of the effective circulating volume, which can be described as that portion of the ECF that fills the vascular a compartment and is “effectively” perfusing the tissues. It is monitored by sensors that are located both in the vascular system and the kidney.
The sympathetic Nervous system and the renin-angiotensin-aldosterone system function in the regulation of sodium balance by the kidneys. It responds to changes in arterial Perseus and blood volume by adjusting the glomerular filatratio rate and the rate at which sodium is filtered from the blood. It also regulates renal reabsorption of sodium and renin release. The renin-angiotensin II and aldosterone system exerts its action through angiotensin II and aldosterone. Angiotensin II acts directly on the renal tubules to inc sodium reabsorption. Also acts to constrict renal blood vessels, dec the glomerular filtration rate and slowing renal blood flow so that less sodium is filtered and more is absorbed. Angiotensin II is also a powerful regulator of aldosterone, a hormone secreted by the adrenal cortex. Aldosterone acts to inc sodium reabsorption by the kidneys, while inc K+ elimination.
What is thirst and disorders of thirst?
Like appetite and eating, thirst and drinking are two separate entities. Thirst is the conscious sensation of the need to obtain and drink fluids high in water contents. Thirst is controlled by two stimuli for true thirst based on water need; 1. Cellular dehydration caused by an inc in ECF osmolatality, 2. A dec in effective circulating volume, which may or may not be associated with a dec in serum osmolality. Sensory neurone, osmoreceptors, which are located in or near the thirst center in the hypothalamus, respond to changes in ECF osmolality by swelling or shrining. A change of 1-2%. Stretch receptors in the vascular a system that monitor the effective circulating volume also aid in the regulation of thirst. It’s one of the earliest symptoms of hemorrhage. 3. The production of angiotensin II by the renin-angiotensin mechanism in the kidney, function in the production of nonosmotic thirst. Angiotensin II inc in response to low blood volume and low BP. It is considered a backup system
Hypodipsia - represents a dec in the ability to sense thirst. Water deficit is commonly associated with lesions in the area of the hypothalamus eg head trauma, meningiomas, occult hydrocephalus subarachnoid hemorrhage. There is also evidence that thrist is dec and water intake reduced in elderly persons, despite higher serum sodium and osmolality levels.
Polydipsia - or excessive thirst, is normal when it accompanies conditions of water deficit, but abnormal when it results in excess water intake, Inc thirst and drinking behaviour can be classified into two categories 1. Inappropriate or false thirst that occurs despite normal levels of body water and serum osmolality,2. Compulsive water drinking . Inapropriate or excessive thirst may persist despite adequate hydration. It is a common complaint with person with congestive heart failure and chronic kidney disease. It is unclear the cause but could be increased angiotensin II levels. Psychogenic polydipsia involves compulsive water drinking and is usually seen in person with psychiatric disorders, most commonly schizophrenia. The causes is uncertain but it usually increases drinking water when they are having periods of exacerbation of their psychotic symptoms. It might be compounded by their antipsychotic meds that increase ADH levels and interfere with water excretion by the kidneys. As well as smoking also stimulates ADH. ,
Whats anitdiuretic hormone and disorders of anti diuretic hormone?
The anti diuretic hormone, vasopressin. Controls the reabsorption of water by the kidneys. The hormone is a small peptide, nine amino acids in length, that is synthesized by cells in the Spurs optic and paraventricular nuclei of the hypothalamus and then transported along a neural pathway to the posterior pituitary gland, where it is stored. When they are stimulated by increased serum osmolality or other factors, nerve impulses travel down the hypothalamic hypophyseal tract to the posterior pituitary gland, causing the stored ADH to be released into the circulation. ADH levels are controlled by ECF volume and osmolality. Osmoreceptors in the hypothalamus sense change in ECF osmolality and stimulate the production and release of ADH. Osmolality and stretch receptors release ADH. Antidiuretic hormone exerts is effects through vasopressin receptors located in the collecting tubules of the kidney. In the presence of ADH, highly permeable water channels called aquaporins are inserted into the tubular membrane. The increased water permeability allows water from the urine filtrate to be reabsorbed into the blood. The abnormal synthesis and release of ADH occurs in a number of stress situation including severe pain, nausea, trauma, surgery, certain anesthetic agents, and some narcotics. Some that affect are nicotine, which stimulates its release, and alcohol, which inhibits it.
Diabetes insipidus - DI is caused by a deficiency of ADH or a decreased renal response to ADH. Persons with DI are unable to concentrate their urine during periods of water restriction and they excrete large volumes of urine, usually 3-20 L/day, depending on the degree of ADH deficiency or renal insensitivity to ADH. The large urine output is accompanied by excessive thirst. The danger arises when the condition develops in someone who is unable to secure the needed water In such cases, inadequate fluid intake rapidly leads to increased serum osmolality and hypertonic dehydration.
Two types; neurogenic or central DI, which occurs because of a defect in the synthesis or release of ADH, and nephrogenic DI, which occurs because the kidneys do not respond to ADH. It is caused by inflammatory, autoimmune, or vascular diseases that affect the hypothalamus - neurohypophyseal system, with less than 10% attributed to heritage forms of the disorder. Loss of 80% of ADH secretory neurone is necessary before polyuria becomes evident. Most people with neurogenic have an incomplete form of the disorder and retain some ability to concentrated their urine. Temp neurogenic DI may follow traumatic head injury or surgery near the hypothalamic hypophyseal tract. It is characterized by impairment of urine-concentrating ability and free water conservation.
Congenital nephrogenic DI, which is present at birth, is caused by defective expression of the renal vasopressin receptors or vasopressin insensitive water channels. Acquired forms of the disorder may occur with pyelonephritis, lithium toxicity, and electrolyte disorders, such as potassium depletion or chronic hyperccalcemia, that interfere with actions of ADH
Manifestation of DI include complaints of intense thirst, a craving for ice water and polyuria or excessive urination, The volume of ingested fluids may range from 2 to 20L daily with corresponding large urine volumes. Partial DI usually presents with less intense thirst and should be suspected in person with enuresis or bed-wetting. May present with hypernatremia and dehydration, especially in persons without free access to water or with damage to the hypothalamic thirst center and altered thirst sensation.
Management of neurogenic DI depends on the cause and severity of the disorder. Many persons with incomplete neurogenic DI maintain near-normal water balance when permitted to ingest water in response to thirst. Pharmacological preparations of ADH are available for persons who cant be managed by conservatism s measures. Both respond partially to thiazide diuretic are thought to act by inc sodium excretion by the kidneys, leading to ECF volume contraction, a dec in the glomerular filtration, and an inc in sodium and water reabsorption.
Syndrome of Inappropriatae antidiuretic hormone - results from a failure of the negative feedback system that regulates the release and inhibition of ADH. In persons with this syndrome, ADH secretion continues even when serum osmolality is decreased, causing marked water retention and dilutional hyponatremia. The SIADH can occur as an acute transient condition or as a chronic condition. Stimuli such as surgery, pain, stress, and temperature changes are capable of stimulating ADH through the CNS. Drugs induce SIADH in different ways, some are thought to increase hypothalamic production and release of ADH, and others are believed to act directly on the renal tubules to enhance the action of ADH. More chronic forms of SIADH may result from lung tumours, chest lesions, and CNS disorders. Tumor s particularly bronchogenic carcinomas and cancers of the lymphoid tissue, prostrated, and pancreas, are known to produce and release ADH independent of normal hypothalamic control mechanisms. Other intrathoracic conditions, such as advanced tuberculosis, severe pneumonia and positive pressure breathing, can also causes SIADH. The suggested mechanisms in positive pressure ventilation is activation of baroreceptors that respond to marked changes in intrathoracic pressure. Disease and injury of CNS can cause direct pressure on or direct involvement of the hypothalamic posterior pituitary structures. Ex brain tumours, hydrocephalus, head injury, meningitis, and encephalitis. HIV can cause SIADH.
Manifestations are those of dilutional hyponatremia. Urine output decreases despite adequate or increase fluid intake. Urine osmolality is high and serum osmolality low. Hematocrit, serum sodium, and BUN levels are decreased because of the dilutional effects of an expanded blood volume. The severity of symptoms is usually related to the extent of sodium depletion and water intoxication.
Treatment - of SIADH depends on its severity. In mild cases, treatment consists of fluid restriction. If that is not sufficient, diuretics such as mannitol and furosemide may be given to promote diuretics and free water clearance. Lithium and the antibiotic demeclocycline inhibit the action of ADH on the renal collecting ducts and sometimes are used in treatment. In severe cases of water intoxication a hypertonic 3% sodium chloride solution may be given IV.
What are disorders of water and sodium balance?
They can be divided into two main categories 1. Isotonic contraction or expansion of the ECF volume brought about by proportionate changes in sodium and water, 2. Hypotonic dilution or hypertonic concentration of the ECF brought about by disproportionate changes in sodium and water. Isotonic disorders usually are confined to the ECF compartment, producing a contraction or expansion of the interstitial and vascular fluids. Disorders of sodium concentration produce a change in the osmolality of the ECF with movement of water from the ECF compartment into the ICF compartment or from the ICF compartment (hyponatremia)into the ECF fluid compartment (hypernatremia).
Isotonic Fluid volume deficit - is characterized by a decrease in the ECF, including the circulating blood volume. Which results when water and electrolytes are lost in isotonic proportions, is almost always caused by a loss of body fluids and is often accompanied by a decrease in fluid intake. This form of volume loss may follow a variety fo disorders, including the loss of GI fluids ex severe vomiting, diarrhea, or GI suction; excessive urinary losses, ex occurs with osmotic diuretics or injuudicious use of diuretic therapy; excessive sweating due to fever and exercise; or endocrine disorders, such as adrenal insufficiency, in which reduced levels of aldosterone cause excessive sodium loss in the urine.
Manifested by a decrease in ECF volume, as evidenced by a decrease in body weight. Thirst is a common symptom, although not always present in early stages, Urine output decreases and urine osmolality and specific gravity increase as ADH levels rise because of a decrease in vascular volume. The decrease fluid is removed from the interstitial spaces the tissue turgor is effected, should when pinched the skin should go back to normal but a 3-5% loss will cause the tissue to remain elevated for several seconds. Arterial and venous volumes decline during periods of fluid deficit, as does filing of the capillary circulation, cap refill will be slower. When it becomes severe, signs of hypovolemic shock and vascular a collapse appear.
Treatment of fluid volume deficit consists of fluid replacement and measure to correct the underlying cause. IV. Isotonic electrolyte solutions are used
Isotonic fluid volume excess - which represents an isotonic expansion of the ECF comparaatment with increases in both interstitial and vascular volumes, usually results from an increase in total body sodium that is accompanied by a proportionate increase in body water. Although it can occur as the result of excessive sodium intake, it is most commonly caused by a decrease in sodium and water elimination by the kidney.ex renal function disorders, heart failure, liver failure, and corticosteroid hormone excess. A condition called circulatory overload results from an increased in blood volume; it can occur during infusion of IV fluids or transfusion of blood if the amount or rate of administration is excessive. Heart failure produces a decrease in the effective circulating volume and renal blood flow and a compensatory increase in sodium and water retention. Liver failure impairs aldosterone metabolism and decreases effective circulating volume and renal perfusion. Corticosteroid hormones also inc sodium reabsorption by the kidneys Cushing syndrome.
Manifested by an increase in interstitial and vascular fluids, and is characterized by weight gain over a short period of time. As vascular volume increases, central venous pressure increases, leading to distended neck veins, slow emptying peripheral veins, a full and bounding pulse, and an increase in central venous pressure. There is often a dilutional decrease in hematocrit and BUN levels due to expansion of the plasma volume. When excess fluid accumulates in the lungs, complaints of SOB and difficult breathing, respiratory crackles, and a productive cough. As items and pleural effusion may occur with severe fluid volume excess.
Treatment - focuses on providing a more favourable balance between sodium and water intake and output. Sodium - restricted diet is often prescribed as a means of decreasing extra cellular sodium and water levels. Diuretic therapy is commonly used in increase sodium elimination.
Two more disorders of water and sodium balance cont.?
Hyponatremia - is usually defined as a serum sodium concentration of less than 135 mEq/L. One of the most common electrolyte disorders. Age related events contribute to it including a decreases in renal function accompanied by limitations in sodium conservation. Can present as a hypovolemic, euvolemic, or hypervolemic state. Can also present as a hypertonic hyponatremia resulting from an osmotic shift of water from the ICF to the ECF, In this situation, the sodium in the ECF becomes diluted as water moves out of body cells in response to the osmotic effects of the elevated blood glucose level. Hypovolemic hypotonic hyponatremia is the most common type. It occurs when water is used to replace the loss of iso-osmotic body fluids. Causes are excessive sweating in hot weather, particularly during heavy exercise, which leads to loss of salt and water. It develops when water, rather then electrolyte-containing liquids are used to replace fluids lost in sweating. GI fluid loss and infection of excessively diluted formulae are common causes of acute hyponatremia in infants and childreen. It also can be a complication of adrenal insufficiency, in which a lack of aldosterone increases renal losses of sodium and a cortisol deficiency leads to increased release of ADH with water retention. Euvolemic hypotonic hyponatremia represents retention of water with dilution of sodium while maintaining the effective circulatory volume within a normal range. A result of SIADH. Hypervolemic hypotonic hyponatremia occurs in edematous states such as decompensated heart failure, advanced liver disease, and renal disease. MDMA esthetician can lead to severe neurological symptoms including seizures, brain edema, and her nation during to severe hyponatremia.
Manifestations - depend on the rapidity of onset and the severity of the sodium dilution. The signs and symptoms may be acute s in severe water intoxication, or more insidious in onset and less severe, as in chronic hyponatremia. Produces an increase in intracellular water, which is responsible for many of the clinical manifestation of the disorder; muscle cramps, weakness, and fatigue reflect the effects of hyponatremia on skeletal muscle function and are often early signs. GI such as nausea and vomiting, abdominal cramps, and diarrhea may occur. The cells of the brain and nervous system are the most seriously affected by increase in intracellular water, symptoms include apathy, lethargy and headache, which can progress to disorientation, confusion, gross motor weakness, and depression of deep tendon reflexes, Seizures and coma occur when serum sodium levels reach extremely low levels.
Treatment - of hyponatremia is determines by the underlying causes, severity and timing of onset. When caused by water intoxication, limiting water intake or discontinuing medications that contribute to SIADH. Administration of saline solution orally or intravenously may be needed when caused by sodium deficiency. Symptomatic hyponatremia may be treated with hypertonic saline solution and a loop diuretic, such as furosemide, to increased water elimination. This combinataion allow for correction of serum sodium levels while ridding the body of excess water. Vasopressin receptor antagonist (vaptans) may be used in the treatment of euvoleic hyponatremia. Severe hyponatremia varies depending on the timing of the onset of the disorder. If prolonged water intoxication is longer then 48 hrs brain cells reduce their concentration of osmolytes as a means of preventing an increase in cell volume. Treatment measures that produce rapid changes in serum osmolality may cause a dramatic dec in brain cell volume. Osmotic demyelination syndrome is characterized by destruction of the myelin sheath of the axons passing through the brain stem. Can cause serious neurological injury and sometimes death.
Hypernatremia - is characterized by a serum sodium level about 145 mEq/L and a Serena osmolality greater than 295 mOsm/kg H2O. Because s sodium and its attendant anion if functionally an impermeable solute, hypernataremia increases ECF toxicity, causing movement of water out of the ICF, resulting in cellular dehydration. It can present as an s gold if state, in which water from the ICF pulled into the ECF preventing a change in volume; as a hypovolemic state, in which water loss is greater than sodium loss; or as a hypervolemic state if there is an addition of a hypertonic solution containing both sodium and water. It develops when there is impaired ability of the kidneys to conserve water by producing concentrated urine, most commonly due to acute or chronic renal failure. Net water loss can occur through the urine, GI tract, lungs or skin. It can result from increase losses from the respiratory tract during fever or strenuous excercise, of from the GI tract due to watery diarrhea or when highly osmotic tube feeding are given with inadequate amounts of water.
Manifestations - caused by water loss are largely those of ECF loss and cellular dehydration. The severity of signs and symptoms is greatest when the increase in serum sodium is large and occurs rapidly, Body weight is dec in porportion to the amount of water that has been lost. Thirst is an early symptom of water deficit, Urine output is dec and urine osmolality inc because of renal water conserving mechanisms. Body temp is frequently elevated, and the skin becomes warm and flushed. Produces an inc in serum osmolality and results in water being pulled out of body cells. As a result, the skin and mucous membranes become dry and salivation and lacrimation are decreased. The mouth becomes dry and sticky and the tongue becomes rough and fissured. Swallowing is difficulty. Movement of water out of the CNS causes decreased reflexes, agitation, headache, and restlessness. Coma and seizures may develop.
Treatment - includes measures to treat the underlying cause of the disorder, and fluid replacement therapy to treat the accompanying dehydration. Fluids can be given orally or IV. Oral glucose - electrolyte replacement solutions are widely available in grocery stores and pharmacies. One serious aspects of sustained hypernatremia is dehydration of brain and nerve cells. The treatment of sustained hypernatremia requires controlled gradual correction of sodium and water levels to avoid serious neurological complication. Same as hyponatremia brain cells protect against changes if correctly to rapidly before the osmolytes have had a chance to dissipate the plasma may become relatively hypotonic in relation to brain cell osmolality. If this occurs water moves into the brain cells, causing cerebral edema and potentially severe neurological impairment.
What is potassium balance regulation? Factors that influence the ECF/ICF shift in K+?
I+ is the second most abundant cation in the body, with 98% located in the intracellular compartment, primarily in skeletal muscle. Of the remaining 2% that is in extracellular compartment, only about .4% is measurable in the plasma. Is maintained at a fairly narrow serum concentration of 3.5 to 5.0 mEq/L.
Balance is normally regulated by dietary intake, urine output, and transcompartmental shifts between ICF and ECF compartments. The kidneys are the main source of potassium loss, with the remainder being lost in the stools from the gastrointestinal tract and in sweat from the skin. It’s filtered in the glomerulus, reabsorbed along with sodium and chloride in the thick ascending loop of henle, and then secreted into the late distal and collecting tubules for elimination in the urine. It is mainly controlled by its secretion from the blood into the tubulars filtrate rather than through its reabsorption from the tubular filtrate into the blood. Aldosterone plays an essential role in regulating K+ elimination in the distal tubule of the kidney. In the presence of aldosterone Na+ is transported back into the blood and K+ is secreted in the tubular filtrate for elimination in the urine.
There is also a K/H exchange mechanism in the collecting tubules of the kidney. When serum K levels increase, K+ is secreted into the urine and H+ is reabsorbed , leading to a dec in pH and metabolic acidosis; when K levels are low, K+ is reabsorbed and H+ is secreted in the urine, leading to an inc in pH and metabolic alkalosis.
Are serum osmolality, acid-base balance, insulin, and inc sympathetic nervous system activity. An acute inc in serum osmolality causes water to move out of the cell; this in turn prompts an inc in K+ concentration that causes it to move out into the ECF.
In metabolic acidosis H+ moves into body cells for buffering, causing K+ to leave and move into the ECF. Both insulin and epinephrine inc cellular uptake of K+ by increasing the activity of the Na+/k+ ATPase membrane pump
What Is critical of K? Whaat does it do? Changes in serum K levels?
K is critical to many body functions, including maintenance of the osmotic integrity of cells, acid-base balance, and the intricate chemical reactions that transform carbohydrates into energy and convert amino acids to proteins. Also in conducting nerve impulses and controlling the excitability of skeletal, cardiac, and smooth muscle.
It does this by regulating the resting membrane potential, the opening of sodium channels that as control the flow of current during the action potential, and the rate of repolaraization. Changes in nerve and muscle excitability are particularly important in the heart, where alterations in serum K levels can produce serious cardiac arrhythmia s and conduction defects.
The resting membrane potential is determined by the ration of ECF to ICF K concentration. A dec in ECF K concentration causes the resting membrane potential to become more negative, moving it further from the threshold for excitation. Thus, it takes a greater stimulus to reach the threshold potential and open the sodium channels that are responsible for the action potential. An inc in serum K has the opposite effect; it causes the resting membrane potential to become mor positive, moving it closer to the threshold.
What is hypokalemia?
Refers to a dec in serum K levels below 3.5 mEq/L. Can be grouped into 3 categories inadequate intake; excessive gastrointestinal, renal and skin losses and a shift between the ICF and ECF compartments. See p178 if needed
Manifestations - include alterations in neuromuscular, gastrointestinal, renal and cardiovascular function. They reflect the effects of it on the electrical activity of excitable tissues such as those of the neuromuscular sysstems as well as the body’s attempt to regulate ECF K levels within a more normal range. The signs and symptoms seldom develop until serum K levels have fallen to less than 3.0 mEq/L. They are typically gradual onset, and it may go undetected. Urine output and plasma osmolality are inc, urine specific gravity is dec, and complaints of polyuria, no Turks, and thirst is common. Metabolic alkalosis and renal chloride wasting are signs of severe. Numerous with GI function, including anorexia, nausea, and vomiting. GI smooth muscle can cause constipation, abdominal distension, and severe hypokalemia, paralytic ileus. Complaints of weakness, fatigue and muscle cramps, Muscle paralysis with life-threatening respiratory insufficiency can occur with severe hypokalemia. In chronic muscle atrophy may contribute.
Most serious effects are on the heart. It produces a dec in the resting membrane potential, causing prolongation of the PR interval. It prolongs the rate of ventricular repolarization and lengthens the relative refractory period, causing depression of the ST segment, flattening of the T wave, and appearance of a prominent U wave. It also increases the risk of digitalis toxicity in persons being treated with the drug and there is an inc risk of ventricular arrhythmias, particularly in persons with underlying heart disease
Treatment - when possible, hypokalemia caused by a K deficit is treated by increasing the intake of foods high in K content- meats, dried fruits, fruit juices and bananas. Oral K supplements are prescribed for person whose intake of K is insufficient. Especially useful in persons who are receiving diuretic therapy and those who are taking digitalis. It may be given IV if oral not tolerated or when rapid replacement. Magnesium deficiency may impair K correction
What is Hyperkalemia? What are the three main causes?
Refers to an increase in serum levels of K in excess of 5.5 mEq/L. It seldom occurs in healthy persons because the body is extremely effective in preventing excess K accumulation in the extracellular fluid.
- Decreased renal elimination 2. A shift in K from the ICF to ECF compartment, 3. Excessively rapid rate of administration.
Cause of serum K excess mostly is decreased renal function , with chronic kidney disease, some kidney disorders such as sickle cell nephrophaty, lead nephropathy, and systemic lupus nephritis. Mineralocorticoid deficiency, which increases tubular reabsorption of K in the distal renal tubule, is another cause of hyperkalemia. Acidosis tends to increase serum K levels by causing K to move from the ICF to the ECF. Tissue injury also causes release of intracellular K into the ECF compartment. Burns and crushing injuries cause cell death and released of K into the extracellular fluids. Transient hyperkalemia may occur during exhaustive exercise of seizures, when muscle cells are permeable to K. Can also be from excessive ingestion or IV. It is normally hard to increase the level of K intake to the level when renal function is adequate and the aldosterone Na+/K+ exchange system is functioning
Manifestations - the signs and symptoms of K excess are closely related to a dec in neuromuscular excitability are absent until the serum concentration exceeds 6 mEq/L. The first symptom associated with it typically is paresthesia ( a feeling of numbness and tingling). Complaints of generalized muscle weakness or dyspnea secondary to respiratory muscle weakness. The most serious effect is on the heart. It decreases membrane excitability, producing a delay in atrial and ventricular depolarization and it increases the rate of ventricular repolarization. As the serum K concentration rises, there is a characteristic sequence of changes in the ECG that are due to the effects of Hyperkalemia on atrial and ventricular depolarization (represented by the P wave and the QRS complex)and repolarization( represented by the T wave and QRS complex). The earliest ECF changes are peaked and narrowed T waves and a shortened QT interval, which reflect abnormally rapid repolarization. Becomes prominent when the serum K concentrataion exceeds 6 mEq/L. If it continues to rise, delayed depolarization of the atria and ventricles produces furthers changes in the ECG. There is a prolongation of the PR interval; widening of the QRS complex with no change in its configuration; and decreased amplitude,widening and eventual disappearance of the P wave. The heart rate are terminal events. Ventricular fibrillation and Cardiac arrest are terminal events.
Treatment - varies with the degree of increase in serum K and whether there are ECG and neuromuscular manifestations. On an emergent basis, calcium antagonizes the K induced decrease in membrane excitability, restoring excitability toward normal. The protective effect of calcium administration is usually short lived and must be accompanied by other therapies to decrease the ECF K concentration. The redistribution of K from the ECF into the ICF compartment can be accomplished by the administration of sodium bicarbonate, B-agonist or insulin to rapidly decrease the ECF concentration, or insulin to rapidly decrease the ECF concentration. Less emergent focus on decreasing or curtailing K intake or absorption, increasing renal excretion, and increasing cellular uptake. Patients with kidney failure may require hemodialysis.
What is calcium phosphorus, and magnesium balance?
They are the major divalent cations in the body. Most are deposited in bone, with only a small amount in the ECF. Homeostatic mechanisms that regulate serum calcium and phosphorus levels are intestine, kidney and bone, principally through the complex interaction of parathyroid hormone and vitamin D. PTH is to maintain ECF calcium concentrations. It does this by stimulating the release of calcium and phosphorus from bone into the ECF; increasing renal reabsorption of calcium and excretion of phosphorus; and enhancing the gastrointestinal absorption of calcium and phosphorus through its effects on vitamin D synthesis. Vitamin D which functions as a hormone, is synthesized by the slin and converted to its active form, calcitriol, in the kidney. The effect the feedback regulation. It stimulates the absorption of calcium and to a lesser extent phosphorus, from the intestine; it increases calcium and phosphorus reabsorption by the renal tubules; and it inhibits PTH synthesis by the parathyroid glands.
Disorders of Calcium Balance? REgulation of calcium balance?
Calcium is the major divalent cation in the body. 99% of body calcium is found in bone, where it provides strength and stability for the skeletal system and serves as an exchangeable source to maintain ECF calcium levels. Most of the remaining calcium is located in the ICF, and only .1% and .2% is present in the ECF. Extracellular calcium exists in three forms: 1. Protein bound, 2.complexed and 3. Ionized. 40% of serum calcium is bound to plasma proteins, mainly albumin. Another 10% is complexed with substances such as citrate, Phosphorus and surface. The remaining 50% is present in the ionized form, only this form is free to leave the vascular compartment and participate in cellular functions. Since most of the protein bound calcium combines with albumin, total serum calcium is significantly altered by serum albumin levels. Ionized CA++ serves a number of functions it participates in many enzyme reactions; exerts an important effect on membrane potentials and neurone excitability; is necessary for contraction in skeletal, cardiac and smooth muscle; participates in the release of hormones, neurotransmitters, and other chemical messengers; influences cardiac contraction th and automaticity by way of slow calcium channels; and is essential for blood coagulation.
Calcium enters the body through the GI tract, is absorbed from the interesting under the influence of vitamin D, excreted by the kidney, and stored in bone. 35% of dietary calcium is absorbed from the duodenum and upper jejunum; the remainder is eliminated in the stool. It is stored in bone and excreted by the kidney. The ionized form of CA++ is filtered from the plasma into the glomerulus and then selectively reabsorbed back into the blood. The distal convoluted tubule is an important regulatory site for controlling the amount of Ca++ that enters the urine. Parathyroid hormone and possibly vitamin D stimulate Ca++ reabsorption in this segment of the nephron. Thiazide diuretics, which exert their effects in the distal convoluted tubule, enhance Ca++ reabsorption. Another factor that influences Ca++ reabsorption by the kidney is the serum concentration. Of phosphorus. An inc in serum phosphorus stimulates PTH, Which increases Ca++ reabsorption by the renal tubules, thereby reducing Ca++ excretion. The opposite occurs with reduction in serum phosphorus levels.
What is hypocalcemia?
Represents a total serum calcium level of less than 8.5 mg/dL and an ionized Ca++ level of less the 4.6 mg/dL. A pseudohypocalcemia is caused by hypoalbuminemia. It results in a decrease in protein bound rather than ionized Ca++ and usually is asymptomatic. The most common causes is abnormal losses of calcium by the kidney, impaired ability to mobilize calcium from bone due to hypoparathyroidism, and increased protein binding or chelation such that greater proportions of calcium are in the nonionized form.Renal failure, in which decreased production of activated vitamin D and hyperphosphatemia both play a role. Decreased levels of PTH may result from primary or secondary forms of hypoparathyroidism. Suppression of PTH released may also occur with elevated levels of vitamin D. Magnesium deficiency inhibits PTH release and impairs the action of PTH on bone resorption. This form of hypocalcemia is difficult to treat with calcium supplementation alone and requires correction of the magnesium deficiency. IT is also a common problem in acute pancreatitis in which fat necrosis and precipitation of calcium soaps produce a decrease in serum calcium. Conditions that alter the ratio of protein bound to ionized calcium can also produce signs of hypocalcemia. This can occur in situation where an increase in pH, like alkalosis, produces a decrease in Ca++. ex hyperventilation sufficient to cause respiratory alkalosis can produce a decrease in Ca++ sufficient to cause tetany. Free fatty acids also increase protein binding, causing a reduction in Ca++. This may occur during stressful situations that cause elevations of epinephrine, glucagon, growth hormone, and adrenocorticotropic hormone levels. It has also been associated with many drugs, including those that inhibit bone resorption, cause vitamin D deficiency or resistance, increase urinary losses or calcium or increase urinary losses of calcium (loop diuretics) or deft calcium absorption through reduced gastric acid production.
Manifestations - can be acute or chronic. Mild are asymptomatic, large or abrupt changes in ionized calcium lead to inc neuromuscular excitability and cardiovascular effects. Ionized calcium stabilizes neuromuscular excitability, thereby making nerve cells less sensitive to stimuli. Nerves exposed to low ionized calcium levels show dec thresholds for excitation, repetitive responses to a single stimulus and in extreme cases, continuous activity. Severity of manifestations depends on the underlying cause, felicity of onset, accompanying electrolyte disorders, and extracellular pH. Increased neuromuscular excitability can manifest as paresthesias (tingling around the mouthed and in the hands and feet) tetany(muscle spasms of the muscles of the face, hands and feet), and in server laryngeal spasm and seizures. Chvostek (is elicited by tapping the face just below the temple at the point where the facial nerve emerges - this causes a spasm of the lip, nose or face) and trousseau (the BP cuff is inflated to 10 mm Hg above systolic bP for 3 minutes, contraction of the fingers and hands indicates the presence of tetany)tested can be used to assess for inc neuromuscular excitability. Cardiovascular effects of acute hypocalcemia include hypotension, cardiac insufficiency, cardiac arrhythmias(heart block and ventricular fibrillation) and failure to respond to drugs such as digitalis, norepinephrine and dopamine.
Treatment - acute is an emergency situation, requiring prompt treatment. IV infusion containing calcium is used when tetany or acute symptoms are present or anticipated because of a dec in the serum calcium level. Chronic is treated with oral intake of calcium of carbonate, Gluck are or lactate salts may be used. Long term treatment may require the use of Vitamin D preparations, especially in persons with hypoparathyroidism and chronic kidney disease. The active form of vitamin D is administered when the liver or kidney mechanisms needed for hormone activation are impaired. Synthetic PTH can be administered by subcutaneous injection in hypoparathyroidism.
What is hypercalcemia?
Represents a total serum calcium concentration greater than 10.5 mg/dL. Occurs when calcium movement into the circulation overwhelms calcium regulatory hormones or the ability of the kidney to remove excess calcium ions. Two most common causes are increased bone resorption due to hyperparathyroidism and neoplasms. Less common causes are increased intestinal absorption of calcium, excessive doses of vitamin D, or the effects of drugs such as lithium and thiazide diuretics. Prolonged immobilization of bone and release of calcium into the bloodstream. Intestinal absorption of calcium can be increased by excessive doses of vitamin D or as the result of a condition called the milk alkali syndrome it is caused by the ingestion of calcium and absorbable antacids, particularly calcium carbonate. A variety of drugs elevate calcium levels. Lithium to treat bipola r disorders has been shown to cause hyperparathyroidism and hyper calcemia. the thiazide diuretics inc calcium reabsorption in the distal convoluted tubule of the kidney.
Manifestations - the signs and symptoms of calcium excess reflect a decrease in neural excitability, alterations in cardiac and smooth muscle function, and exposure of the kidneys to high concentration of calcium. There may be a dulling of consciousness, stupor, weakness, and muscle flaccidity. Behavioural changes may range from subtle to personality to acute psychoses. The heart responds to eke water levels of calcium with inc contractility and ventricular arrhythmias. Digitalis accentuates these responses. GI symptoms include constipation, anorexia, nausea, and vomiting, reflecting a dec in smooth muscle activity. Bone pain can occur with hyperparathyroidism or malignancy. Excess PTH can lead to bone reabsorption with development of bone cysts or osteoporosis. High calcium concentrations in the urine filtrate impair the ability of the kidneys to concentrate urine by interfering with the action of ADH. This causes salt and water diuretics and inc sensation of thirst. Also predisposes to the development of renal calculi. Pancreatitis is another potential complication and is probably related to stones in the pancreatic ducts. Hypercalcemic crisis describes an acute lifethreatening inc in the serum calcium level. Hyperparathyroidism and malignant disease are the major causes. Has polyuria, excessive thirst, dehydration, excessive muscle weakness, cardiac arrhythmias, disturbed mental state, and altered levels of consciousness
Treatment - is usually is directed toward rehydration and use of measures to inc urinary excretion of calcium and inhibit release of calcium from bone. The excretion of sodium is accompanied by calcium excretion. Diuretics and sodium chloride can be administered to inc urinary elimination of calcium after the ECF volume has been restored. Loop diuretics commonly used rather than thiazide diuretics, (which inc calcium reabsorption). After lowering the calcium levels is followed by measures to inhibits bone reabsorption. Drugs are used to inhibit calcium mobilization include bisphosphonates ( which act mainly by inhibiting osteoclastic activity, provide a significant reduction in calcium levels with relatively red side efffects), calcitonin (inhibits osteoclastic activity, thereby dec bone resorption), and corticosteroids( inhibit the conversion of vitamin D to its active form and are used to treat hypercalcemia due to vitamin D toxicity and hematologist malignancies).
What are disorders of phosphorus balance? Regulation of phosphorus balance?
Is mainly located in bone 85% and in the ICF 14%. Only about 1% is in the ECF compartment and of that’s, only a minute proportion is in the plasma. Normal serum phosphorus level ranges from 2.5 - 4.5 mg/dL. Levels in children are higher.
It is ingested in the diet and eliminated in the urine. Comes from milk and meats and others. 50-65% is absorbed in the intestine, jejunum. Absorption is diminished by concurrent ingestion of substance that bind phosphorus, including calcium, magnesium and aluminum. Renal elimination is then regulated by an overflow mechanism in which the amount of phosphate lost in the urine is directly related to phosphate concentration in the blood. It exists in two forms within the body inorganic and organic. Inorganic is the one measured by lab.
It is essential to many bodily functions - it plays a major role in bone formation; is essential to a number of metabolic processes, including the formation of ATP and the enzymes needed for glucose, fat, and protein metabolism, is a necessary component of several vital parts of the cell, being incorporated into the nucleic acids of DNA and RNA and the phospholipids of the cell membrane; and serves as as acid-base buffer in the ECF and in the kidney. Delivery of oxygen by the rbc depends on organic phosphorus in ATP. Also needed for normal function of WBC and platelets.
What is hypophosphatemia?
Is commonly defined by a serum phosphorus level of less than 2.5 mg/dL in aduts; and is considered severe of less than 1.0 mg/dL. It may occur despite normal body phosphorus stores as a result of movement from ECF into the ICF compartment. Serious depletion may exist with low, normal or high plasma concentrations. Most common causes are depletion of phosphorus because of insufficient intestinal absorption, transcompartmental shifts, and inc renal losses. Often it involves more then one. Food intake is usually adequate. It may be inhibited by administration of glucocorticoids, high dietary levels of magnesium, and hypothyroidism. Prolonged ingestion of antacids may also interfere. It can cause inc phosphate losses in the stool. Malnutrition inc phosphate excretion and phosphorus loss from the body. Catabolic events that occur with diabetic ketoacidosis also deplete phosphorus stores. It usually doesn’t become apparent until insulin and fluid replacement have reversed the dehydration and glucose has started to move back into the cell. Chronic alcohol use is common cause. Respiratory alkalosis due to prolonged hyperventilation can produce hypophosphatemia through inc PTH levels and inc phosphate excretion. Clinical conditions associated with hyperventilation include sepsis, withdrawal from chronic alcoholism, fever and primary hyperventilation.
Manifestation - Manyof phosphorus deficiency result from a dec in cellular energy stores associated with a deficiency in ATP and impaired oxygen transport due to a dec in RBC. The decc in cellular energy can cause altered neural function, disturbed musculoskeletal function, and hematologist disorders. RBC metabolism is impaired by phosphorus deficiency; causing the cells to become rigid, undergo inc hemolysis, and have diminished ARP and 2,3 DPG levels. Chemotactic and phagocytosis functions of WBC and hemostatic functions of the platelets are also impaired. Anorexia and dysphasia can occur, neural manifestation (intention tremors, paresthesias, hypo reflexes, stupor, coma and seizures) are uncommon but serious. Chronic depletion interferes with mineralization of newly formed bone matrix. In growing children, this process causes abnormal endochondral growth and clinical manifestations of rickets. In adults leads to joint stiffness, bone pain,, and skeletal deformities consistent with osteomalacia.
Treatament is usually directed toward prophylaxis. Can be accomplished with dietary sources high in phosphorus milk or IV replacement solutions. Supplements are contraindicated in hyperparathyroidism, chronic kidney disease and hypercalcemia because of risk of extracellular calcificaations.
What is Hyperphosphatemia?
Represents a serum phosphorus concentration in excess of 4.5 mg/dL in adults. Moderate exists when serum phosphate is in the range of 4.6 - 6.0 mg/dLand severe greater then 6.0. Can regulate from failure of the kidneys to excrete excess phosphate, rapid redistribution of intracellular phosphate to the ECF compartment, or high phosphate intake. Because it eliminates in kidney is common in impaired renal function. Release of intracellular phosphorus can result from conditions such as massive tissue injury, rhabdomyolysis, heats stroke, K deficiency, and seizures. Administration of excess phosphate containing antacids, laxatives, or enemas , especially when there is a dec in vascular volume and reduced glomerular filtration rate. Serious and even fatal has reportedly resulted from administration of phosphate enemas.
Manifestations - many of the signs and symptoms of excess are related to a calcium deficit because of the reciprocal relaxation ship between calcium and phosphorus levels, a high serum phosphate level tends to lower serum calcium levels, which can lead to tetany and other signs of hypocalcemia. Inadequately treated hyperphosphatemia in chronic kidney disease can lead to renal bone diesease, and extra lessons calcification in soft tissues. A secondary effect of chronic kidney disease is stimulation of modular hyperplasia of the parathyroid glands that results in a secondary hyperparathyroidism.
Treatment - is directed at the cause of the disorder. Dietary restriction of foods that are high in phosphorus may be used. Calcium-based phosphate binders are useful in chronic hyperphosphatemia. Sevelamer may be used as a effective as a calcium -based binder, but lacks it adverse effects. Hemodialysis is used to reduce phosphate levels in chronic.
