Clinical Approach to Electrolyte Disorders

Question 1

Most potassium is where?

Answer 1

Muscle and IC

Question 2

What increases and decreases serum K

Answer 2

HYpo - insulin, alpha antagonists and beta agonists alkalosis

Hyper - acidosis, hyperglycemia, beta 2 antagonist and alpha agonists, increase in osmolarity and exercise

Question 3

Regulation of collecting duct K secretion

Answer 3

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)

Question 4

Hypokalemia levels

Answer 4

Under 3.5
Moderate under 3
Severe under 2.5

Question 5

Causes of hypokalemia

Answer 5

First consider pseudo (K falls in test tube)

True - inadequate intake, shifts into cells, GI losses, renal losses)

Question 6

Pseudohypokalemia

Answer 6

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

Question 7

Decreased oral postassium intake

Answer 7

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

Question 8

IC shift causing hypokalemia

Answer 8

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

Question 9

Renal loss

Answer 9

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

Question 10

Diuretic induced

Answer 10

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

Question 11

Hypokalmeia sx and signs

Answer 11

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)

Question 12

Tx of hypokalemia

Answer 12

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

Question 13

Causes of hyperkalemia

Answer 13

Psuedo

True - increased intake

IC to EC shift

Decreased renal excretion

Over 5.4

Question 14

Pseudohyperkalemia

Answer 14

Hemolysis
Warm temp
Fragility
Severe leukocytosis or thrombocytosis
Fist clenching/tourniquet

Question 15

Increased intake

Answer 15

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

Question 16

Hyperkalemia EC shift

Answer 16

Hyperosmolarity - DKA and hyperglycemia

Drugs - beta blockers, digoxin, succinylcholine

Acidemia

^all if membrane intact

If membane not intact - rhabdomyolysis, tumor lysis syndrome, hemolysis

Question 17

Decreased renal excretion - hyperkalemia

Answer 17

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)

Question 18

Consequences of hyperkalemia

Answer 18

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

Question 19

Tx of hyperkalemia

Answer 19

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

Question 20

Forms of calcium and phosphate

Answer 20

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

Question 21

PTH and calcitrol

Answer 21

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

Question 22

What stimulates 1alpha hydroxylase

Answer 22

Low serum phosphate and PTH

Too much vitamin D and serum phosphate along with FGF 23 will suppress 1 alpha hydrozylase

Question 23

Calcium phosphate homeostasis

Answer 23

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

Question 24

Hypercalcemia clinically

Answer 24

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

Question 25

Causes of hypercalcemia

Answer 25

TPH excess Excessive hormone indepednet bone resroption Vit D excess Excessive dietayr Ca Increased renal Ca rebasorption

Question 26

PTH excess and horomone independent causes

Answer 26

PTH - hyperparathyroidism (adenoma), PTH secreting malignancy (squamous cell of the lung), lithium, familial hypocalcuric hypercalcemia ID - osteolytic bone metastases, immobilization, Pagets, hyperthyroidism

Question 27

Vit D excess Excessive Ca intake INcreased renal Ca reabsorption

Answer 27

Ectopic calcitrol production...sarcoidosis Milk alkali syndrome Thiazides

Question 28

Dx eval of hypercalcemia

Answer 28

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

Question 29

Tx of hypercalcemia

Answer 29

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

Question 30

Hypocalcemia clinical

Answer 30

NM irritability Paresthesia, muscle twitching, largospasm, shortnes of breath Cehck Chvostek's sign and Trousseuas sign Prolonged QT interval

Question 31

Causes of hypocalcemia

Answer 31

Decreased Ca intake Vit D deficiency PTH deficiency

Question 32

PTH def causes

Answer 32

Thyroidectomy or PTdectomy AI hypoparathyroidism Infiltration of PTH Hypomagnesemia PTH resistance

Question 33

Vit D def

Answer 33

Low clacidiol - low intake, inadequeate exposure, malapsorption Decreased conversion of calcidiol to calcitrol - advanced chronic kidney dz Calcitriol resist - Vit D resistant rickets

Question 34

Other hypocalc causes

Answer 34

Osteoblastic bone matasases, pancreatitis, hungry bones syndrome, multiple trnasfusion,s bisphosphonates, acute resp alkalosis, hyperphosphatemia (TLS, rhabdo)

Question 35

Dx of hypocalcemia

Answer 35

Assess serum phosphorus Vit D def - low Low PTH - high Renal failure - High

Question 36

Hypocalcemia with increased PTH

Answer 36

Renal failure Ca loss from circulation - pancreatits or tumor lysis Vit D def or resistance PTH resistance (dec Mg or sepsis)

Question 37

Hypocalcemia tx

Answer 37

Symp - IV calcium Asym - oral calc Correct vit D or Mg def

Question 38

Hyperphos clinical

Answer 38

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

Question 39

Causes of hyperphosphatemia

Answer 39

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

Question 40

Dx of hyperphosphatemia

Answer 40

Work up the likely concurrent clacium disorders If 1,25 D production decreased then decreased intestinal PO4 absorption Will have high FGF 23 levels

Question 41

Tx of hyperphos

Answer 41

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

Question 42

Hypophos clinical

Answer 42

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

Question 43

Causes of hypophos

Answer 43

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

Question 44

Hypophos dx evaluation

Answer 44

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

Question 45

Tx of hypophos

Answer 45

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

Question 46

HyperMg clinical

Answer 46

CV - bradycardia, conduction block and hypotension NM - decreased reflexes, muscle weakness, drowsiness, coma, PS blockade

Question 47

Cuase of hyperMg

Answer 47

Renal failure, acromegaly, familail hypocalcuric and hypercalcemia Adrenal insuffiency

Question 48

Tx of hyperMg

Answer 48

Cessation of mag administraiton Admin of calcium in sever esx hypermagnesemia IV saline and furosemide Dialysis

Question 49

Hypomag clinical

Answer 49

General weakness, NM hyperexcitability wit hyperrelxeia CSpasm Should have co-hypocalcemia and hypokalemia Prolonged GT, ST depresison, ventriclular arrythimos, digoxin toxicty

Question 50

Causes of hypomagnesemia Dec GI uptake

Answer 50

Poor intkae, H+ pump inhibitors, primary intestinal hypomag Excessive GI losses as well

Question 51

Renal losses and misc mechs for hypomag

Answer 51

Meds Hypercal or hypokal Osmotic diuresis Transirent renal tubular dysfunction (alcohol) Familai renal Mg wasting syndromes - Gitelman syndrome Pancreatitis and hungry bones syndrome

Question 52

HypoMg tx

Answer 52

Oral if no sx Iv is sx and arrhytmia Cautious in renal fialure