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TL Phosphorus
hyperphosphatemia/ hypophosphatemia
| Question | Answer |
|---|---|
| What is the primary anion found in intracellular fluid? | phosphorus |
| 85% | Percent of the body’s phosphorus found in bone and teeth |
| 14% | Percent of the body’s phosphorus found in soft tissues |
| 1% | percent of the body’s phosphorus found in ECF |
| What are cell membranes made of? | phospholipids |
| What are the functions of phosphorus in the body (C, M&Nf, Mcfp, O, B,A, B&T)? | Cell membrane integrity (phospholipids), Muscle and neurologic function, metabolism of carbs, fats, and protein, promotes 02 delivery from RBCs, Buffers acids and base, part of ATP, building block of bone/teeth |
| Give four broad mechanisms that contribute to phosphorus levels in the body. | Intake, hormones, Kidneys, transcellular shifts |
| What is the RDA for phosphorus? | 800 to 1200 mg/day |
| Where is phosphorus mostly absorbed in the GI? | Jejunum |
| What do the kidneys do if there is too much phosphorus? | excrete phosphorus |
| What do the kidneys do if there is not enough phosphorus? | hang on to phosphorus |
| About how much of the phosphorus absorbed in the jejunum is excreted through the kidneys? | 90% - the rest goes out through the GI tract. |
| What is a normal range for phosphorus? | 2.5 to 4.5 mg/dl or 1.8 to 2.6 mEq/L |
| Name 8 dietary sources of phosphorus (DDEFNOPW). | Dairy, Dried beans, Eggs, Fish, Nuts/seeds, Organ meats, poultry, whole grains |
| How does PTH work to lower phosphorus? | First it cause the realease of calcium and phosphorus from the bones. Both levels rise initially. Then it causes the kidneys to excrete phosphorus – lowering the phosphorus level. |
| What effect does reduced PTH have on the kidneys in regards to phosphorus? | Allows for phosphorus to be reabsorbed. |
| If calcium is high phosphorous is what? | low |
| What kind of relationship exists between calcium and phosphorus levels? | inverse |
| A patient who has hypophosphatemia will probably also have what condition? | hypercalcemia |
| What effect does insulin have on phosphorus? | Moves it into cells. |
| Name 2 things that insulin moves into cells. | phosphorus and glucose |
| Name 2 things that insulin moves into cells. | phosphorus and glucose |
| Why does severe hypophosphatemia put our patients at risk for organ failure? | Phosphate is part of ATP – when the body does not have enough, it cannot support its energy needs. |
| Hypophosphatemia is considered severe when serum levels are below what? | 1mg/dl |
| What are the three underlying mechanisms that lead to hypOphosphatemia? | Shift from EFC to IFC, Decreased intestinal absorption, increased excretion from the kidneys |
| What effect does respiratory alkalosis have on serum phosphorus levels? | Respiratroy alkalosis causes phosphorus to shift from EFC to IFC causing hypophosphatemia |
| Elevated serum glucose level | Hyperglycemia |
| How does hyperglycemia cause hypophosphatemia? | by causing the release of insulin which transports phosphorus as well as glucose into cells, and by osmotic diuresis/electrolyte loss |
| What is “refeeding syndrome” and when does it typically occur? | A syndrome that develops about three days after the initiation of enteral or parenteral feeding insufficient in phosphorus. Phosphorus leaves the EFC and enters the IFC. |
| Name several things that can inhibit phosphate absorption from the GI (MS, S, A, S, V, L, D). | malabsorption syndromes, starvation, antacids that bind with phosphorus, sucralfate, lack of Vit. D, Laxative abuse, diarrhea |
| What is sucralfate used for? | Active duodenal ulcers |
| What is the most common cause of phosphorus loss through the kidneys? | Diuretics |
| Which diuretics are most commonly the cause of hypophosphatemia? | Loop, Thiazide and acetazolamide |
| Name 4 types of drugs that are associated with hypophosphatemia(DIAL)? | Diuretic, Antacids, Insulin, Laxatives |
| What’s this stuff? Aluminum Carbonate, Aluminum hydroxide, Calcium carbonate, Magnesium oxide | antacids that can lower serum phosphate levels |
| How does diabetic ketoacidosis cause hypophosphatemia? | High blood sugar and ketones cause osmotic diuresis resulting in phosphorus loss from the kidneys |
| How does hyperparathyroidism cause hypophosphatemia? | PTH causes the kidneys to excrete phosphorus. |
| What patients with what type of injury are at risk for hypophosphatemia? | Severe burns |
| What are the signs and symptoms of mild to moderate hypophospatemia? | Usually none |
| Why isn’t poor diet usually to blame for hypophosphatemia? | because phosphate is found in most foods |
| The main cause of phosphate loss from the kidneys is diuretics. What is the second most common cause? | Diabetic Ketoacidosis |
| How does ethanol affect phosphate? | Causes the kidneys to excrete more phosphate |
| What is 2,3-DPG? | A compound in the Red Blood Cells that promotes oxygen delivery from the RBCs to the tissues |
| What happens when there is a shortage of 2,3-DPG? | RBCs have a greater affinity for oxygen than other cells. Without 2,3-DPG to help them let go of it, the RBCs retain O2. Less oxygen is delivered to tissues. |
| Why does hypophosphatemia affect 2,3-DPG? | The P in 2,3-DPG stands for phosphorus. Gotta have phosphorus to have 2,3-DPG. |
| What is the most common sign of hypophosphatemia? | muscle weakness |
| Give 9 signs and symptoms associated with hypophosphatemia (mw, ss, c, h, dco, r, c, and rf). | Muscle weakness, slurred speech, cardiomyopathy, hypotension, decreased cardiac output, rhabdomyolysis, cyanosis, and respiratory failure |
| How is mild to moderate hypophosphatemia treated? | Oral supplements or increased dietary intake |
| How is severe hypophosphatemia treated? | I. V. phosphorus (potassium phosphate or sodium phosphate) |
| What’s Neutra- Phos? | phosphate supplement |
| What is the rate for potassium phosphate? | Requires slow administration – no more than 10 mEq/hr |
| What are two possible complications associated with I.V. phosphate replacement? | hyperphosphatemia and hypocalcemia |
| Does hypocalemia make muscles and reflexes act more like Droopy or Taz? | Taz |
| How does insulin work? | It is the taxi that takes glucose from the blood to the cells for use as energy. |
| Where does insulin come from? | Beta cells in the islets of Langerhans in the pancreas |
| What hormone from the pancreas release stored glucose from liver to the blood? | Glucagon |
| Where does Glucagon come from? | The alpha cells in the islets of Langerhans in the pancreas |
| Causes the liver to convert stored glycogen into glucose which is released into the blood stream | Glucagon |
| Raises glucose levels in the blood | Glucagon |
| Lowers glucose levels in the blood | Insulin |
| Makes glucose available | Glucogon |
| Takes glucose from the blood to the cells that use it | Insulin |
| What are ketones? | an acidic by product of fat metabolism |
| How do ketones cause problems in diabetic ketoacidosis? | They are acid so they lower pH causing acidosis. They have an osmotic diuretic effect adding to dehydration/electrolyte loss caused by the osmotic effect of high blood sugar. |
| What is the focus of nursing care for a patient with hypophosphatemia (3)? | careful monitoring, safety measures and interventions to restore normal serum phosphate levels |
| Name some dangerous conditions that may develop in patients with hypophosphatemia (RF, LCO, C, S, C). | Respiratory Failure, Low cardiac output, Confusion, Seizure, Coma |
| Why do we need to check and document the LOC and neurological status of our patient with hypophosphatemia every time we check vital signs? | because any changes in the patient’s neurologic status need to reported to the HCP right away - Confusion, seizure, coma are potential complications. |
| How do we care for our patient in with hypophosphatemia in regards to potential respiratory effects? | Monitor rate and depth of respirations; Report signs of hypoxia – confusion, restlessness, increased respiratory rate, cyanosis; Prevent hyperventilation; Monitor ABGs and pulse oximetry; wean slowly from ventilator |
| Our patient with severe hypophosphatemia may be in danger of heart failure due to reduced myocardial function. What signs do we watch for (4)? | crackles, SOB, Decreased BP and Elevated heart rate |
| Why are patients with hypophosphatemia at greater risk for infection? | The lack of ATP results in decreased WBC function |
| How do we monitor and protect our patient with hypophosphatemia in regards to infection? | check temp every 4 hours, Check WBC counts, Follow strict sterile technique when changing dressing, Report signs of infection. |
| How will we know if our patient with hypophosphatemia is losing muscle strength? | Frequently test the strength of the patients hand grasp and watch for slurred speech. |
| What is an adverse effect of phosphate supplements? | diarrhea |
| How can we improve the taste and the absorption of phosphate supplements? | Give them with juice (taste) and Vitamin D (absorption). |
| What are some things we need to keep in mind if our patient is receiving phosphorous by IV (3)? | Infuse slowly with an infusion device (no more than 10 mEq/L). Watch for signs of hyperphosphatemia/hypocalcemia (TAZ). IV site – Patent/no infiltration – Phosphorous can cause tissue sloughing and necrosis |
| How can we protect our patient’s safety in regards to potential neurological effects of hypophospahtemia? | Help with ambulation and ADLs. Keep essential objects near the patient so they don’t have to travel. Bed in lowest position with side rails up (and padded if seizures are a risk). Keep an artificial airway at the patient’s bedside. |
| Our patient’s family is concerned because their family member with hypophosphatemia isn’t making any sense. What can we tell them? | Confusion caused by a low phosphorus level is only temporary and will likely decrease with therapy. |
| What are two especially important lab values to watch for a patient with hypophosphatemia? | Calcium and phosphorus. |
| Name some things we could keep in our patient’s sight to help with orientation? | Clocks, calendars, and familiar personal objects (family pictures). |
| Name 12 things we should document when our patient has hypophosphatemia (VS, I, NS, MS, RA, PLV, N, I, S, I, S, PT)? | Vital Signs; I&0; Neurologic Status; Muscle Strength; Respiratory Assessment; Pertinent Lab Values; HCP notifications; IV – site, medication, does, pt response; Seizures; Interventions and pt response; Safety measures; Pt teaching |
| Why would renal failure result in hyperphosphatemia? | It is the job of the kidneys to excrete phosphorus. Healthy kidneys usually excrete the amount of phosphorus absorbed from the GI tract. |
| What is the normal glomerular filtration rate per minute? | 125 mL/minute |
| At what glomerular filtration rate are the kidneys unable to excrete phosphorus fast enough to maintain normal phosphorus levels? | When the filtration rate falls below 30mL/min the kidneys are not able to filter excess phosphorus adequately. |
| Why would we be concerned about hyperphosphatemia in a patient who has had thyroid or parathyroid surgery? | A risk of these types of surgeries is hypoparathyroidism. PTH is a hormone that tells the kidneys to release phosphorus. Levels will rise in its absence. |
| Give two common examples of acid-base imbalances that cause phosphorus to shift from ICF to ECF. | Respiratroy Acidosis and DKA |
| How could chemotherapy cause hyperphosphatemia? | Cell destruction causes phosphorus to shift from ICF to ECF. |
| Anything that cause _______ ________ can trigger a shift of intracellular phosphorus to ECF. | Cell destruction |
| Give 6 examples of conditions that cause cell destruction(C, MN, R, I, HS, T). | Chemotherapy, muscle necrosis, rhabdomyolysis, infection, heat stroke, and trauma |
| How do laxatives cause hyperphosphatemia? | Some (like Fleet enemas) contain phosphorus. |
| Name 2 ways that a patient could have excessive intake of phosphate. | Overuse of phosphate supplements or laxatives/ enemas that contain phosphorus |
| What does cow’s milk have to do with hyperphosphatemia? | Babies can get hyperphosphatemia from cow’s milk because it has high levels of phosphorus and infants have higher levels of phosphorus than adults anyway. |
| Name 4 drugs associated with hyperphosphatemia (E, L, P, V). | Enemas (Fleet enemas), Laxatives with phosphate, phosphorus supplements ( oral or parenteral), Vitamin D supplements |
| Hyperphosphatemia doesn’t cause much trouble on its own, so why do we care about it? | Because of the inverse relationship between phosphorus and calcium - Hypocalcemia can be life threatening. |
| What type of paresthesia is typical of hyperphosphatemia/HypOcalcemia? | Paresthesia may start at the finger tips and around the mouth. It may spread to the face and along the limbs. |
| What might a patient with hyperphosphatemia/hypocalcemia experience in their muscles and reflexes (SMS, C, P, W, PC&T, H, T)? | Severe muscle spasm, cramps, pain, and weakness; positive Chvostek’s and Trouseau’s sign, hyperreflexia; Tetany |
| What neurologic signs are associated with hyperphosphatemia/HypOcalcemia? | decreased mental status, delirium, and seizures |
| What ECG changes would we expect with hyperphosphatemia/HypOcalcemia? | Prolonged QT interval and ST segment |
| What signs and symptoms would a patient with hyperphosphatemia/HypOcalcemia have related to the cardiovascular and GI systems? | hypotension, heart failure, anorexia, N&V |
| What is calcium phosphate? | An insoluble compound that is formed when calcium and phosphorus bind |
| A condition that results from the precipitation of calcium phosphate into soft tissues related to chronically high phosphorus levels | Calcification |
| Calcification | A condition that results from the precipitation of calcium phosphate into soft tissues related to chronically high phosphorus levels |
| Why would we be concerned about organ dysfunction related to chronically high phosphate levels? | Calcification of organs like the heart, lungs, or kidneys may cause dysfunction. |
| What are some signs and symptoms of calcification related to the heart, lungs, kidneys, eyes, and skin? | irregular heart rate or arrhythmias, dyspnea, oliguria, corneal haziness, conjunctivitis, cataracts, impaired vision, papular eruptions |
| Give 5 lab values that would be consistent with hyperphosphatemia (P, C, X, B, E, ). | serum phosphorus above 4.5 mg/dL (2.6 mEq/L), serum calcium below 8.5 mg/dL, X-ray Skeletal changes (if chronic), BUN above 25mg/dL (worsening renal function), ECG prolong QT and ST |
| What is the goal of treatment for a patient with hyperphosphatemia? | Fix the cause, correct hypocalcemia |
| How do we treat hypercalcemia that is due to excessive intake? | Reduce intake (laxatives, or supplements) |
| What if dietary changes don’t change the patient’s elevated phosphorus levels? What else could be going on? | Taking phosphorus binding antacids as directed? Using laxatives or enemas with phosphate? Kidneys working? Is there an underlying cause of hyperphosphatemia (bone disorder, infection, tissue damage) |
| Why would a mildly elevated phosphorus levels actually be a good thing for a patient with renal failure? | Phosphate in the form of 2,3 – DPG would help move more oxygen from the RBCs to tissues and offset the effects of chronic anemia on oxygen delivery preventing hypoxemia. |
| Why shouldn’t a patient with renal insufficiency receive magnesium antacids to inhibit phosphorus absorption from the GI? | May cause hypermagnesemia |
| A patient with what condition would probably receive lanthanum carbonate to lower phosphorus absorption? Why? | A patient with end stage renal failure because it does not contain calcium or aluminum, but it binds with phosphorus. |
| What are some drugs that are used to bind with phosphorus and prevent its absorption from the GI tract (AMCG, PBA, CSCA, SH)? | aluminum, magnesium, or calcium gel or phosphate –binding antacids, calcium salts, calcium carbonate, and calcium acetate, sevelamer hydrochloride |
| Why careful dosing is required for calcium salts, carbonate, and acetate? | to prevent hypercalcemia |
| What could be used to help a diabetic patient lower serum phosphate levels? | Insulin causes phosphate to shift into cells |
| How would we treat hyperphosphatemia caused by respiratory acidosis or DKA? | Treat the underlying cause. |
| How is Respiratroy acidosis treated? | Improve ventilation and lower Co2. |
| How is Diabetic ketoacidosis treated? | Fluid and electrolyte replacement and insulin therapy |
| What can be done for patients with severe hyperphosphatemia as long as their kidneys function well and they can tolerate increased fluid volume? | I.V. Saline solution to increase phosphorus excretion from the kidneys. |
| What is acetazolamide? | a proximal diuretic that is sometimes employed to promote excretion of phosphorus |
| What is the “Big guns” treatment for severe hyperphosphatemia with hypocalcemia (especially in the case of renal failure)? | Hemodialysis or peritoneal dialysis |
| What should the focus of our care for patients be for hyperphosphatemia(CM, SM, I)? | Careful monitoring, safety measures and interventions to restore normal serum phosphate levels |
| Why do we watch our patients with hyperphosphatemia for paresthesia around the mouth or the fingertips, hyperactive reflexes, or muscle cramps? | Signs of hypocalcemia – Alert the HCP if these occur. |
| We need to let the HCP know if our patient develops signs of calcification. What are they (O, VI, C, IHRoP, PE)? | oliguria, visual impairment, conjunctivitis, irregular heart rate or palpitations, and popular eruptions |
| Why is it important that we monitor I&O for a patient with hyperphosphatemia? | Because output below 30mL/hour inhibits the kidney’s ability to clear excess phosphorus. |
| What lab values will we watch closely for our patient with hyperphosphatemia? | Calcium, phosphorus, BUN and creatinine |
| Why is it important to monitor BUN and Creatinine levels for our patient with hyperphosphatemia? | Hyperphosphatemia can impair renal tubules when calcification occurs. |
| What can we do to help our patient if they need dietary restriction of phosphorus? | Consult with a dietitian. |
| What things should be documented when our patient has hyperphosphatemia? | Assessment findings; I&O; I.V. therapy and Meds; Muscle Symptoms – spasms, cramps, pain, weakness; paresthesia; Visual disturbances; Safety measures; Notification of HCP; Interventions and response; Pt teaching |
| Why is muscle weakness one of the hallmarks of hypophosphatemia? | Cells use ATP for energy - Especially muscle cells. No phosphate – No ATP |
| Why is it difficult to wean a patient with a phosphorus level below 1 mg/dL from a ventilator? | Severe hypophosphatemia can lead to respiratory muscle weakness making it hard for the patient to breathe on their own. |
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Perseverandovercome
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