Clinical Approach to Electrolyte Disorders Flashcards
Most potassium is where?
Muscle and IC
What increases and decreases serum K
HYpo - insulin, alpha antagonists and beta agonists alkalosis
Hyper - acidosis, hyperglycemia, beta 2 antagonist and alpha agonists, increase in osmolarity and exercise
Regulation of collecting duct K secretion
Distal tubule flow (dependent on upsteam Na reabsorption)…more Na reabsorption means more secretion bc more sodium coming into the cells
MC receptor (alosterone (serum K and RAAS) and GCs)
Hypokalemia levels
Under 3.5
Moderate under 3
Severe under 2.5
Causes of hypokalemia
First consider pseudo (K falls in test tube)
True - inadequate intake, shifts into cells, GI losses, renal losses)
Pseudohypokalemia
Cell K uptake in the test tube
Due to very high number of metabolically active cels (AML or CML)
Temp increases Na-KATPase and shifts K into cells
Often also associated with pseduohypoglycemia
Prevent by rapidly separating plasma and cells or store blood at 4C
Decreased oral postassium intake
Rarely sole
Causes more total body K depletion than hypokalemia
Contributing factor in other primary etiologies of hypokalemia
Urinary K losses can go as low as 10 mmol/day
Could be found in pts with eating disorders
IC shift causing hypokalemia
Alkalosis - small effect
INsulin
Increase B2-adrenergic (stress induced reelease, theophulline, albuterol)
Thyroid hormone (thyrotoxic periodic paralysis)
Anabolism (tx of pernicious anemia…rapidly expanding cell mass like leukemia or lymphoma)
Hypokalemia periodic paralyssis
Hypothermia
Renal loss
Primary hyperaldosteronism - adrenla hyperplasia or adenoma
Secondary hyperaldosteronism - diruetics, vomiting, salt wasting neprhopathies
Potassium wasting neprhopathies - hypermagnesemia, drug toxicity, polyuria, RTA
Mineralocorticooid excess - Cushing syndrome, licorice
Diuretic induced
INceased tubular flow
Increased sodium delivery so reabsorption through the ENaC
Enhanced tubule negative charge in tubule
Induce volume depletion and aldosterone secretion
All of this leads to increased K secretion
Hypokalmeia sx and signs
Due to hyperpolarization
PVCs, abnormal EKG (prolonged QT, U-wave), digitalis toxicity
Fatigue, weakness, paralysis and rhabdo
Rudced motility (constipation)
POlyuria and polydipsia due to renal concentring defect (mild nrphogenic DI)
Tx of hypokalemia
Oral KCl for mild to moderate
IV KCl for severe or sx…in slaine, NOT glucose to prevent insulin induced IC shift of insulin
Replace Mg if needed
Causes of hyperkalemia
Psuedo
True - increased intake
IC to EC shift
Decreased renal excretion
Over 5.4
Pseudohyperkalemia
Hemolysis Warm temp Fragility Severe leukocytosis or thrombocytosis Fist clenching/tourniquet
Increased intake
Unusual cause of hyperkalemia if there is no renal failure
Enteral supplements, salt subs, blood transfusions, penicillin, dialysate
Take a good hx…highest content (dried figs, molasses, seaweed)
Very high - nuts, beans
High content - tomatoes, potetatoes, bananas, oranges
People who are on sodium restriciton often have risk factors for hyperkalemia
Hyperkalemia EC shift
Hyperosmolarity - DKA and hyperglycemia
Drugs - beta blockers, digoxin, succinylcholine
Acidemia
^all if membrane intact
If membane not intact - rhabdomyolysis, tumor lysis syndrome, hemolysis
Decreased renal excretion - hyperkalemia
Primary decrease in tubular flow and distal Na delivery
Primary decrease in MC activity
Abnormal cortical collecting duct
Loss of GFR will decrease sodium delivery (renal failure, ECF depletion and renal vasoconstrction)
Anything that blocks the ENaC channel (traimterene, amiloride, trimethoprim)
Hypoaldosteronsim (drugs, diabetes, type 4 RTA, adrenal insufficient, congential)
Consequences of hyperkalemia
Muscle weakness and paralysis
ECG changes and arrhythmias
Increase EC potassium reduces MC excitability
Increased potassium leads to suppression of trhe SA node and conduction by the AV node
Tx of hyperkalemia
Goal is to prevent arrhythmia
Based on the way the way that hyperkalemia occurred
Calcium stabilizes the cardiac membranes
Shift potassium into cells with insulin, bicarb, or beta2 agonist
Increase excretion with cation exchange resin/polymer or slaine, diuretics, dialysis
Forms of calcium and phosphate
Calcium - 45% is freely ionized…if albumin is low, more is ionized because amount bound to protein is lower….calcium corrected=measured+(.8(4-albumin))
Most of phosphate is in the bones…remainder is IC…small fraction in serum is phospholipids and inorganic phosphate…consides of HPO4 and H2PO4
PTH and calcitrol
PTH - from PT glands…increase calcium and decreased phosphorus
Calcitrol - from diet or cholestrol precursor with UV light…activated in liver and kidney…increease calcium and phosphorus
What stimulates 1alpha hydroxylase
Low serum phosphate and PTH
Too much vitamin D and serum phosphate along with FGF 23 will suppress 1 alpha hydrozylase
Calcium phosphate homeostasis
Bone formation inhibited by PTH
Bone resoprtion - activated by PTH and calcitrol and inhibited by calcitonin
Calcitriol increase reabsorption of Ca and phosphate in kidnyes…PTH blocks reasorption of phosphate but increases calcium…FGF23 blcoks phsophate uptake in kidneys
Hypercalcemia clinically
Stones - neprholithiasis
Bones - bone pain
Groans - ab pain
Psychiatric overtones - confusion, depression, anxeity
Other sx could be constipation, weakenss, lethargy, anorexia
Renal insuffiency, distal RTA, NDI, dehydration
Short QT interval
Causes of hypercalcemia
TPH excess
Excessive hormone indepednet bone resroption
Vit D excess
Excessive dietayr Ca
Increased renal Ca rebasorption
PTH excess and horomone independent causes
PTH - hyperparathyroidism (adenoma), PTH secreting malignancy (squamous cell of the lung), lithium, familial hypocalcuric hypercalcemia
ID - osteolytic bone metastases, immobilization, Pagets, hyperthyroidism
Vit D excess
Excessive Ca intake
INcreased renal Ca reabsorption
Ectopic calcitrol production…sarcoidosis
Milk alkali syndrome
Thiazides
Dx eval of hypercalcemia
Measure PTH…if high, measure 24 hr urinary calcium excretion…high then priamary hyperPTH, low then familai hypocalcuric hyperclacemia
If low or normal, measure PTHrP, calcidiol, and calcitrol…PTHrP evelated - malignancy
Elevated calcidiol - excessive intake of calcium of Vit D
Elevated calcitrol with normal calcidiol - ectopic calcitriol production
None of 3 elevated - bone mets, consider rare cases
Tx of hypercalcemia
IV hydration with saline solution
Loop diuretics (after volume normal) - inhibits renal Ca reabsortpion
Bisphos and calcitonin to inhibit bone resorption
Steroids in ectopic production of calcitrol - granulomatous dz and lymphoma
Hypocalcemia clinical
NM irritability
Paresthesia, muscle twitching, largospasm, shortnes of breath
Cehck Chvostek’s sign and Trousseuas sign
Prolonged QT interval
Causes of hypocalcemia
Decreased Ca intake
Vit D deficiency
PTH deficiency
PTH def causes
Thyroidectomy or PTdectomy
AI hypoparathyroidism
Infiltration of PTH
Hypomagnesemia
PTH resistance
Vit D def
Low clacidiol - low intake, inadequeate exposure, malapsorption
Decreased conversion of calcidiol to calcitrol - advanced chronic kidney dz
Calcitriol resist - Vit D resistant rickets
Other hypocalc causes
Osteoblastic bone matasases, pancreatitis, hungry bones syndrome, multiple trnasfusion,s bisphosphonates, acute resp alkalosis, hyperphosphatemia (TLS, rhabdo)
Dx of hypocalcemia
Assess serum phosphorus
Vit D def - low
Low PTH - high
Renal failure - High
Hypocalcemia with increased PTH
Renal failure
Ca loss from circulation - pancreatits or tumor lysis
Vit D def or resistance
PTH resistance (dec Mg or sepsis)
Hypocalcemia tx
Symp - IV calcium
Asym - oral calc
Correct vit D or Mg def
Hyperphos clinical
Leads to hypocalcemia and stimulation of PTH
Manifestations related to hypocalcemia
Deposition of phosphate and calcium in soft tissues
Acute severe can cause neprhopathy or renal failure
Causes of hyperphosphatemia
INcreased GI intake - laxatives
Dec urinary excretion - renal failure, familial tumoral calcinosis, hypoPTH, VIt D excess, acromegaly
Internal redistribution - TUmor lysis syndrome, rhabdo, lactic acidosis
Dx of hyperphosphatemia
Work up the likely concurrent clacium disorders
If 1,25 D production decreased then decreased intestinal PO4 absorption
Will have high FGF 23 levels
Tx of hyperphos
INtact renal function and acute - result on own…or saline with acetazolamide
IMapired renal function - dialysis
Intact chornic - tx underlying
Impaired - low phosphate diet and phosphate binders
Hypophos clinical
Early - muscle weakness, dec MC contractility, encephalopathy, increased affinity of Hgb for O2
Dec bone mineralizaiton, bone pain
Late - rhabdo, resp failure, HF, seizures, hemolysis, osteomalacia
Causes of hypophos
Dec GI absorption - dec intake, malabsorption, phosphate binderes
Inreased urinary excretion Vit D def, hyperparathyroidism, genetic dz, fanconi syndrome, tumor indcued osteomalacia
Internal reidstribtuon - refeeding, hungry bones syndrome, acute resp alkalaosis, durnig tx of DKA or HHS
Hypophos dx evaluation
Check 24 hr phosphate xcretion
High - renal losses…check metabolic panel
Low calcidiol with normal or low calcium…vit D def
Elevated calcium and PTH - hyperpTH
Metabolic acisosis and glucosuria>hyperglycema - Fanconi syndrome
Low output - take a good hx…alcoholism, chronic diarrhea, severe GERN, PTectomy
Tx of hypophos
Over 2 asx - no tx
Sx over 1 or ax 1-2 - oral phsphate repltion
under 1 and sx - IV phosphate, if asx - oral phsophate
HyperMg clinical
CV - bradycardia, conduction block and hypotension
NM - decreased reflexes, muscle weakness, drowsiness, coma, PS blockade
Cuase of hyperMg
Renal failure, acromegaly, familail hypocalcuric and hypercalcemia
Adrenal insuffiency
Tx of hyperMg
Cessation of mag administraiton
Admin of calcium in sever esx hypermagnesemia
IV saline and furosemide
Dialysis
Hypomag clinical
General weakness, NM hyperexcitability wit hyperrelxeia
CSpasm
Should have co-hypocalcemia and hypokalemia
Prolonged GT, ST depresison, ventriclular arrythimos, digoxin toxicty
Causes of hypomagnesemia Dec GI uptake
Poor intkae, H+ pump inhibitors, primary intestinal hypomag
Excessive GI losses as well
Renal losses and misc mechs for hypomag
Meds
Hypercal or hypokal
Osmotic diuresis
Transirent renal tubular dysfunction (alcohol)
Familai renal Mg wasting syndromes - Gitelman syndrome
Pancreatitis and hungry bones syndrome
HypoMg tx
Oral if no sx
Iv is sx and arrhytmia
Cautious in renal fialure
