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TL Phosphorus

hyperphosphatemia/ hypophosphatemia

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.