Transcript Electrolyte Disorders

Electrolyte Disorders
WS04111: WTD3
Water Metabolism
Water intake regulated by:
Thirst is the response to water loss
ADH release center is close to the thirst center
Water loss regulated by:
Proximal renal tubular absorption
(reabsorbs 125 L/day of the 200 L/ day filtered by glomerulus)
Loop of Henle- absorbs sodium and dilutes urine (only sodium is
reabsorbed)
Collecting duct- controlled by ADH- affects the total amount of
urine excreted
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Sodium Imbalance:
Hyponatremia (Low Sodium) (fig.21-1)
 Hypovolemia:Dehydration/ Diarrhea/Vomiting
 Renal Salt loss:Diuretics/ ACE inhibitors
 Hypervolemic:CHF/ Liver disease/
Nephrotic syndrome/ ESRD
(ESRD = end stage renal disease)
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Sodium Imbalance:
Hyponatremia Signs and Symptoms
Mild ones (130-135) usually asymptomatic
(125-130) Nausea and malaise
(115-120) Headache/ Lethargy/ Disorientation
Red flag: seizure/ coma> cardiac arrest/ death
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Sodium Imbalance:
Hyponatremia- Treatment
Replace fluid with iv-0.45% sodium chloride
(half normal saline)
Asymptomatic casesWater restirction
Fludrocortisone
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Hypernatremia
Only when sodium levels are greater than
155clinically significant effects are seen
Decreased fluid intake
Increased skin loss
Increased GI loss (due to loss of water)
Renal- ‘osmotic’ diuresis- (hyperglycemia)/ lack of
ADH
Renal- drugs- lithium
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Hypernatremia- symptoms and signs
Depression, confusion, coma, convulsions
Therapy: Free water by mouth
IV 5% dextrose
Vasopressin/ Thiazides (increase proximal
tubular reabsorption of water- reduces
water delivery to distal tubule and helps)
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Sodium Metabolism
Primary osmotic agent (mostly ECF)
Distal tubule and collecting duct are major
regulators of urinary sodium output
?Hormones- Aldosterone (increases sodium
reabsorption) controlled by Renin- Angiotensin
Atrial natriuretic peptide/ Dopamine/
Prostaglandins- inhibits Na reabsorption
CHF-Liver-Nephrotic syndrome-CRF- Steroid- all
lead to Na retention
Urine sodium excretion less than 20 mEq/L
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Edema Therapy
Restrict dietary sodium (<1 g)
Diuretis- loop diuretics- lasix-potassium
sparing- aldosterone antagonists (Aldactone)
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Electrolyte Disorders
Potassium Metabolism
Potassium Basics
Primarily intracellular (3000 mEq)
Extracellular (65 mEq)
Normal dietary intake 60-90 mEq/day
Kidney preserves potassium homeostasis
Potassium must be driven into the cellsInsulin/ Epinephrine help the drive
Renal- mostly excreted in distal tubule
(controlled by aldosterone)
More sodium delivered to the tubules more potassium
is excreted
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Hypokalemia (low K)
Less than 3.5 mEq/L
GI causes: inadequate intake (<10mEq/day)
diarrhea/ vomiting (loss of volume=
Renin-Angiotensin-Aldosterone-leads to
urinaryK loss)
K redistribution: Insulin therapy/ Epinephrine/
Folic acid/ B12 therapy/ High bicarb intake/ Periodic
paralysis in Asians
– thyroid related:
defective epinephrine sensitivity
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Hypokalemia (low K)
Renal causes: Diuretics/ Penicillins
Adrenal tumors-Aldosteronism/ ectopic ACTH/
Licorice (anise) ingestion- steroid like substance- low
K/ HTN/ alkalosis
Tobacco chewing- same as above
Renin tumors/ Renal artery stenosis
CHF
Magnesium depletion leads to tubular K
wasting
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Hypokalemia signs and symptoms
Neuro-muscular- weakness/ paralysis/
constipation/ ileus/ decreased reflexes/
rhabdomyolysis
Cardiac- arrhythmias (if on digoxin+lasix)/ ECGlow amplitude T wave/ depressed ST segment
Endoctine- pancreatic insulin release
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Hypokalemia Therapy
 Check serum K level
 Administer potassium chloride- iv / oral
 20 mEq oral/day
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Hyperkalemia
Serum K levels greater than 5.5 mEq/L
Causes- Rhabdomyolysis/ tissue trauma/
Acidosis/
Renal failure/
Aldosterone deficiency- lead nephropathy,
therapy/ Addison’s disease
ACEi
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Hyperkalemia Signs and Symptoms
 Dangerous!
 ECG changes happen but not diagnostic (only at
high levels more than 6.5 mEq/L)
 Emergency treatment – Calcium/ Insulin/ beta
stimulants/ dialysis/ Resins
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Electrolyte Disorders
Calcium Metabolism
Hypocalcemia
 Most common cause- advanced CRF/CKD
(decreased vit D3 and hyperphosphatemia)
 Magnesium depletion aggravates low calcium
symptoms
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Hypocalcemia
 Affects muscles and heart
 Muscle spasms-tetany
 Laryngospasms/ oral numbness and tingling
 Chvostek’s sign/ Trousseau’s sign
 IV Calcium gluconate thrapy
 Oral calcium and vit D therapy
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Hypercalcemia More than 12 mg/dL
Hyperparathyroidism/ Cancer related
Thiazide diuretics
Milk-Alkali excess- Tums for calcium use
S&S: Constipation/ Vomiting/ Anorexia/
peptic ulcer/ renal stones/
CNS- drowsiness, lethargy, convulsions,
Medical emergency
coma
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Electrolyte Disorders
Phosphate Metabolism
Phosphate Basics
Dynamic requirement for cell activity (ATP)
Main intracellular buffer
Acid-base action (H and P exchange)
85% in bone
Dietary intake 1200 mg/day800 mg excreted in urine, 400 in feces
PTH regulates P excretion by proximal renal
tubule
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Hypophopshatemia
 Dietary lack- rare (starvation)
 Antacid abuse- binds phosphate in the gut
 Respiratory alkalosis
 Sepsis- due to impaired WBC chemotaxis
 Renal: Diabetes/
Excess PTH increases urine phosphate loss
 Alcoholics- reduced renal threshold
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Hypophopshatemia-features
 CNS- coma, convulsions, peripheral neuritis
 Blood- rare (hemolytic anemia)
 Muscular- ATP deficits- muscle pain
(seen in alcoholics)
 Bone- increased bone resoprtion
 Increased urine phosphate levels
(more than 100 mg/L) suggests renal causes
 Treat with oral phosphate 1500-2000 mg/day
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Hyperphosphatemia
 Renal failure Acute rhabdomyolysis
 Tumor lysis
 Hypoparathyroid
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Hyperphosphatemia features
 Hypocalcemia features-low BP
 ‘Renal osteodystrophy’
 Calcification of soft tissues
 Increased risk of cardiovascular events
 Therapy- dialysis/
 Oral phosphorus binders:
calcium carbonate 500 mg thrice daily
sevelamer hydrochloride 800-1600 mg
daily with meals (adv. No
calcium!)
 Lanthanum carbonate can also be used.
thrice
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Magnesium Basics
 Second most abundant intracellular cation
first)
 50% stored in bone, rest in muscles, less
1% in body fluids
 Acts on myoneural junctions/
 cardiac rhythm defects
 Kidney conserves magnesium
 Plasma levels 1.5-2.5 mEq/L
(K is
than
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Hypomagnesemia
 Malabsorption
 Renal- tubular dysfunction
Drugs-thiazides/lasix/ antibiotics
Hyperaldosteronism
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Hypomagnesemia- features
 Muscle twitiching, tremors, weakness
 Affects renal K reabsorption –
leads to hypokalemia
 Hypocalcemia and hpokalemia may be
associated conditions
 Therapy- oral magnesium- 250-500 mg /day in
divided doses
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Hypermagnesemia
 Seen in advanced renal disease
 Iatrogenic-laxatives/antacids
 Therapy of toxemia of pregnancy
 Features- muscle weakness, depressed tendon
reflexes, ileus, urine retention, low BP
 Lab- low serum Calcium/ ECG changes
 Therapy- calcium- antagonist for magnesium
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Hydrogen ion issues
 Henderson-Hasselbalch!
 (Normal HCO3- 24/Pco2-40)
 pH = 6.1+log HCO3¯
0.3xPco2
 Extracellular pH- 7.4/ Intracellular- 7.0-7.2
 Normal metabolism generates- carbonic acid and ‘noncarbonic’ acids- acetoacetate/ ketone (beta-hydroxy
butyric acid)/sulfuric and phosphoric acids
 Carbonic acid mostly exhaled as CO2
 Non carbonic acids excreted by kidneys
(1 mEq/Kg body wt.)
 Usually require hospital referral
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