Electrolyte Apps Flashcards
Lab measure most useful in determining “renal handling”
Urine (24 hr) or fractional excretion of electrolyte (Fex)
fractional is faster
labs you order in vitamin D deficiency
PTH
Phosphorus
Calcium
Vitamin D
HIGH urine concentration means
renal wasting
LOQ urine concentration means
extrarenal loss of lyte
K is predominantly excreted
via Kidneys
also in sweat, stool
aldosterone effect on k
stimulates K excretion in kidney
hyperaldosterone and [K]
low potassium as a product of normal renin function
increasing sodium reabsorption and potassium excretion
hypoaldosterone and [K]
potassium excess thru sodium and potassium exchange and sodium wasting
heparin and K
inhibits aldosterone production in adrenal glands
THEREFORE: hyperkalemia
MC cause of hypokalemia in developing world
GI losses from infectious diarrhea
concentration in intestinal secretion 10x higher than gastric section
meds known to cause hypokalemia (4)
TZD
loops
Beta agonists
insulin
MC cause of HYPERkalemia
Lab: psedudohyperkalemia
TRUE DZ: Kidney Disease
meds known to cause hyperkalemia
ACE/ARB KCL supplements Spironolactone B Blockers Bactrim, Cyclosporine, Tacrolimus
Hypokalemia lab value
<3.5
CRITICAL: <2.5
hyperkalemia lab value
> 5.5
CRITICAL: >6.5
how to distinguish between renal and non-renal loss
TTKG “Spot potassium excretion”
TTKG > 4 suggest renal loss of potassium
calculation of TTKG
(K urine x OSMserum)/ (OSMurine x Kserum)
safest and easiest mean to provide tx of hypo K
oral potassium
dosing of potassium rise
10mEq of oral K to raise serum by 0.1
how much of human body is made of water? where?
60%
ICF space
pt population most prone to hyperkalemia
renal insufficiency/kidney disease patients
failure to excrete potassium
most salient SE of IV administration of K?
burning sensation in vein
functions of Phosphate (5)
energy metabolism
cell signaling
regulation or protein synthesis
skeletal development
bone integrity
where does phosphate mostly exist?
essential mineral that exists mainly as HYDROXYAPPETITE (bone) or INTRACELLULAR constituent
disease that can provoke elevation in phosphate
CKD
PTH and phosphate renal absorption
DECREASE renal absorption
PTH fxn
increases degradation of hydroxappetite crystals in bone (PO4, Ca release)
allows absorption of Ca and prohibits PO4
what increases absorption of phosphate from GI
Vitamin D
what augments renal absorption of phosphate
growth hormone
most ideal way to obtain serum phosphate las?
fasting
hypophosphatemia causes hypoxia by:
impairs 2,3 DPG
shifts oxyhemoglobin dissociation curve to LEFT
impairs RBC ability to deliver O2 to cells
source of phosphate
Hypo is rare bc it is so common in DIET
processed foods and being absorbed lgrly by passive absorption
most LIKELY source of hypophosphatemia
Hyperparathyroidism
starvation/malabsorption as well
MC population to suffer from malabsorption disorders?
alcoholism
critical LOW phosphate:
<1mg/dL
late that develops and maintains bones
Ca
most abundant mineral in body
NMJ performance and blood coagulation
how is Ca excreted
stool
normal SERUM Ca
8.5-10.5
decrease albumin by 1 gm = decrease Ca by 1 mg
normal ionized Ca
4.6-5.3
serum total calcium + affected by
protein bound (50% of Ca)
availability of serum proteins
ionized Ca
NOT protein bound (45% of Ca)
ACTIVE calcium
ionized Ca and pH (increase or decrease)
elevated pH = decreased ionized Ca
decreased pH = increased ionized Ca
mc of TRUE hypocalcemia
disorders of PTH or Vitamin D
pseudohypocalcemia
hypoalbuminuria
hungry bone syndrome
low phosphorus
low calcium
low magnesium
associated with parathryoidectomy
lab good for determine hypercalcemia from hyperparathyroid and malignancy
PTH
PTrH
malignancy will have DECREASED PTH
magnesium and PTH
hypermagnesemia causes PTH depravation and is not responsive to peripheral tissues
mc cause of HYPERcalcemia
hyperparathyroidism
hypercalcemia and diabetes insipidus
activation of Ca sensing receptors in collecting ducts reduces ADH-induced water permeability
volume depletion worsens hypercalcemia (high water loss increases [Ca])
also causes K loss
electrolyte depletion MC in patients with Albuterol
hypokalemia
shifts potassium into cell at +10mg
K value and pH increase/decrease
pH rise = hypokalemia (alkalosis)
pH loss = hyperkalemia (acidosis)
Mg and other electrolytes
“cornerstone electrolyte”
if it is low, others will be
monitoring in patients with hypoK and hypoMg
continuous cardiac monitoring
admit everyone with critical hypoK
K IV repletion
10 mEq to raise serum by 0.1
IV can’t go more than 10 mEQ/hr, central = 20/hr
if you go faster you may cause death due to arrhythmia)
Loop diuretics and electrolyte derangements
hypomagnesium and hypokalemia
EKG finding most classic for hypoK
T wave: decreased amplitude, brand
U wave
EKG finding most classic for hyper K
peaked T waves
causes of pseudohyperkalemia
cellular lysis (via drawing the blood)
fist clenching during phlebotomy
displaces potassium into cell (moved from ECF to ICF)
insulin
bicarbonate
albuterol
causes potassium excretion from body
loop diuretic
sodium polystyrene
sulfonate (kay-X)
Hemodialysis
drug provided cautiously in patins taking digoxin
calcium glutinate
chloride
STONE heart
agent that req. central line prior to administration
chloride
3x potent of Ca Gluconate (caustic to vein)
pancreatitis and calcium
causes hypocalcemia
combo of necrotic cells and insoluble Ca = fat necrosis
hypocalcemia S/S
SPASM QT
Spasm Peri0oral numbness Abdominal cramps Stridor Mental status change QT prolongation Tetany
classical PE signs of hypocalcemia
Chovstek sign (tapping of facial n.) Trousseau sign (BP cuff, more reliable)
IV Ca
SEVERE hypocalcemia
must provide Mg as well
IV Ca caution in Heart DZ
vasoconstriction and ischemia
esp. w/low CO and peripheral vasoconstriction
PO Ca
calcium given with vitamin D
population of its with hypochloremia
excessive volume depletion
excessive diuresis, vomiting, nasogastric tube suction
tx of hypochloremia
d/x suctioning (underlying cause)
addition of 0.9 NS
torsdaes and Mg
1-2 g in dextrose over 15-20 min
medication used to antagonize Mg
calcium
putting a patient on Lasix, what should you add?
oral potassium chloride
to prevent hypokalemia
vitamin D deficiency clinical presentation
likely caused by CKD
elderly
low calcium and phosphate
Order: Ca, PTH, Vitamin D
milk alkali syndrome
causes Ca depletion and due to taking exogenous Ca/base (tums)
elevated Ca + metabolic alkalosis + AKI
hypercalcemia and fatigue/weight loss
malignancy
Granulomatous disease
endocrinopathies
at risk for cardiac anomalies
bones, stones, groans, moans
bones: osteolysis
stones: kidney stones
groans: pancreatitis, peptic ulcer dz
moans: psychiatric dz
tx of hypercalcemia
IV hydration (force diuresis)
administer bisphosphonates + calcitonin
meds to avoid in hypercalcemia
diuretics - worsens dehydration, potassium, Mg loss
vomiting and electrolyte derangement
chloride depletion
hypochloremia metabolic alkalosis
lab added if pt has dark urine, pain in muscles
Rhabdo– CK levels
low phosphate tx
Admission IV hydration (esp CK elevation)
replete with oral phosphate
parenteral phosphate administration Se
can cause decline in Ca - therefore give oral
most ideal way to tx hyperphosphatemia
targeting underlying cause + phosphate binders (phoslo)
