-
functions
structure of cell membrane, source of high energy bonds in ATP, plays a role in how O2 is released from RBCs
-
distribution
primarily intracellular, critically ill, increased metabolism, increased phosphorus
-
normal serum conc of phos
2.5-4.5 mg/dl, doesn't necessarily reflect total body phosphorus, serum phos varies 2mg/dl over a day due to dietary intake, check serum same time every day
-
regulation of phos
kidney is the major homeostatic regulator, under action of PTH, PTH activiated if increase plasma PO4 or decreased plasma Ca, increased abs if decrease PO4 or serum calc
-
-
decreased renal excretion-hyperphos
acute renal failure, CKD GFR<=30 ml/min
-
increased renal tubular reabsorp-hyperphos
hypopara, growth hormone excess, hyperthyroidism
-
drugs causing hyperphos
phosphate enema(fleet, phospho-soda), phos lax, parenteral/enteral phos admin-can accumulate mostly in mod-severe renal dysfxn, oral phos replacement, vit D toxicity, increase abs of pho
-
cell injur-hyperphos
rhabdomyolysis, TLS(malig) hemolysis, other: diabetic ketoacidosis/lactic acidosis(once tx, will shift back)-shifts from intra to extra
-
acute sx of increase in phos
hypocalc and tetany(binding of ca and phos)
-
chronic sx of increase phos
CaPO$ calcification(once combined, can go to other areas, causes organ damage in soft tissue, eyes, kidneys, vasculature), renal osteodystrophy(renal bond disease)-chronically high PTH levels, risk indicator(higher risk of precipitation): calc phos product >55- serum calcium mg/dl X serum phos mg/dl
-
treatment of acute hyperphos
treat underlying, saline inf(to expand ECF and dilute pho and incr phos exc at 100-200 ml/hr), dextrose + insulin(rarely used, FYI-less effect on phos than K), hemodialysis(if have access)
-
tx of chronic hyperphos
dietary restr <=1g/d total of: dairy products, meats, dried beans, nuts, colas, cocoa, choc
-
phosphate binders
decrease phos abs from GI tract, tk with meals, calc carb and calc acetate also used to increase ca, so don't use if increased, sevelamer(renagel), lanthanum(fosrenol), alum hydroxide(amphogel)(caution in pts with renal impairment, long-term, CNS toxicities) are constipatins
check phos level q 24-48 hrs if in hosp, if severe or cont renal replacement therapy/cont dialysis, may monitor more often
-
hypophos
<2.5 mg/dl, relatively common in ICU
-
etiology of hypophos
alcohol related, inadequate int/abs-starvation malabs(diar, vom, phos antacids), phosphate-binding drugs, sucralfate, steroids(impair conver D2-D3)
-
intracellular phosphate shift-hypophos
refeeding syn, rapid tumor growth, resp alkalosis, insulin, gluc, epi admi, hungry bone syn
-
increased phos excretion-hypophos
vol expansion, hyperparathry, acetazolamide, GCs and sodium bicarb
-
post renal transplant-hypophos
decreased PTH, decreased renal abs, steroid immunosuppressants
-
musculoskeletal manifestations of hyporphos(primary)
weakness, myalgia, resp muscle fat, resp failure, slow weaning from ventilator, osteomala/bone pain, CNS-metabolic encepha
-
Gi manifestations of hypophos(primary)
anor/ileus
-
precautions/CONTRA to tx for hypophos
look at renal fxn <=30ml/min, decrease 50% and consider Ca Phos prod
-
tx of mild-mod hypophos (1.0-2 mg/dl)
oral therapy preferred-1.5-2.0 gm (50-60mM) phos qd divided into 3 or 4 doses
milk(1mg/cc, 1g/L), fleet phospho soda, Neutra-phos and neutra-phos k(most common these two)
monitor serum PO4 qd until desired serum level attained, low end of normal 2.5
-
tx of severe hypophos <1 mg/dl or symptomatic or NPO
parenteral-BE CAREFUL, 15-30 mM PO4 in 250cc D5W or NS over 4-6 hours, MD orders can be confusion
- use sodium phosphate if potassium >4
- use potassium phosphate if potassium <4
infuse slowly(ideally with pump) to avoid hypercalc tetany, HOTN, and acute renal failure (secondadry to CaPO4 precipitating out in kidney)
monitor serum PO4 q 2-4 hrs after dose adminsterd and repeat above dose until serum PO4 >2 mg/dl
-
risks of treatment of hypophos
hypocalc, hyperphos, hyperkale or hypernatre (based on which salt) diarrhea (more with PO) hypomag ( due to intracellular shifting)
|
|