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• 50% of body weight is water in women • 60% of body weight is water in men •
ICF:55-75% • ECF:25-45% including intavascular and extravascular in a ratio of
1:3 Major ECF particles: Major ICF particles: 1-sodium 1potassium 2-chloride 2-
ATP
Water Balance
• Plasma osmolality:275290mosmol/kg • Obligate water loss :Urine-Stool-skin
and respiratory tract. • Minimum urine output of 500 ml/day is required for neutral
solute balance • Water intake must equal water excretion
Water intake
• Thirst osmolality volume or blood pressure increase in effective or decrease in
ECF
Sensed by osmoreceptors
Water excretion
A V P=ADH
Binds to V2 receptors of principal cells in the collecting duct The major stimulus
for secretion is hypertonicity sensed by the osmoreceptors in antrolateral
hypothalamus
Non osmotic factors that regulate AVP 1-effective circulating arterial volume 2-
nausea,pain,stress,hypoglycemia 3-Pregnancy
Hypovolemia
• Definition:”state of combined salt and water loss exceeding intake leading to
ECF volume contraction” NB:The loss of Sodium may be renal or extrarenal Eg
renal: diuretics-glucose-ureamannitoldiuretic phase of acute tubular
Pathophysiology
• ECF volume contraction
Diagnosis:
1-BUN:creatinine=20:1(decreased GFR) However high BUN realtive to creatinine
occurs in hyperalimentation and glucocorticoid therapy. 2-Urine sodium < 20
mmol/L However in ATN there is impaired Sodium reabsorption or in case of
vomitting:see Cl 3-urine osmolality>450 mosmol/kg and specific gravity>1.015
However in DI SG and urine osmolalityare
Treatment
• Mild:correct via the oral route • Severe:IV normal saline(154 mmol/L) However
in Hypenatremia use half normal saline or 5% dextrose Patients with significant
hemorrhage,anemia may require blood transfusion or dextran
Hyponatremia
• Definition:Plasma sodium concentration<135 mmol/L Plasma Osmolality may
be Decreased(hypotonic) Increased (hypertonic) Normal(isotonic)
Hypotonic hyponatremia
• Primary water gain and secondary sodium loss:eg:1-Primary polydipsia 2-beer
potomania 3-SIADH 4-Addison disease and hypothyroidism
Clinical features
Mainly neurological: Brain cell swelling and cerebral edema Symptoms depend
on : The severity of onset and the absolute decrease in plasma Na • Nausea and
Malaise • Headache, lethargy, confusion • Stupor, seizures and coma(plasma Na
<120mmol/L or decreases rapidly)
Diagnosis
1-Plasma osmolality 2-Urine osmolality 3-Urine Na 4-Urine K
Treatment
1-Raise plasma Na by restricting water intake and promoting water loss 2-
Correct the underlying disorder 2 protocols In ECF volume volume contraction In
ECF
In Edematous state
• Restriction of Na and water • Correction of Hypokalemia • Promotion of Water
loss in excess of Na
Correction
(Desired plasma Na –Measured Plasma Na) X Weight X 0.6 in man or 0.5 in
woman
Important:
• Do not raise plasma Na more than 0.5 to 1 mmol/L/hour And no more than 10-
12 mmol/L/day Except in altered mental status and seizures you are allowed up
to 2 mmol/L/hour For fear of developing ODS
Hypernatremia
• Definition: plasma Na concentration >145mmol/L • Hypernatremia is a state of
hyperosmolality which is usually mild unless impaired thirst(Primary hypodipsia)
or limited access to water is present. • Causes: Primary Na gain(rare) or water
deficit(common)
CDI NDI
Clinical features:
• Contracted ICF volume • Decreased brain cell volume increasing risk of
subarachnoid or intracerebal hemorrhage . • Neurologic manifestations: 1-altered
mental status 2-weakness 3-seizures and coma
Treatment
• Stop the ongoing water loss • And correct the water deficit • Correction:
water deficit=[(Plasma Na concentration-140)/140]X TBW • TBW is 40% in
women and 50%in men
• Do not correct more than 0.5 mmol/L/h • AND no more than 12mmol/L/h over
the 24 hours
• The safest route is by mouth or via nasogastric tube • Half normal saline or
dextrose can be given IV • CDI: desmopressin nasally • NDI: Thiazide.
Potassium
• Major intracellular cation • Normal:3.5-5mmol/L • For balance: matching
ingestion with excretion. • Immediately following a meal K⁺ enters cells as result
of insulin and initial elevation of plasma K⁺. • Eventually however excess is
excreted in urine
Potassium excretion
• 90% of filtered K⁺ is reabsorbed by PCT and loop of Henle.(TALH) • K⁺ delivery
to the distal nephron approximated dietary intake • Regulation by
ALDOSTERONE and HYPERKALEMIA
Hypokalemia
• Definition: plasma potassium concentration<3.5mmol/L • Causes 1-decreased
intake 2-shift into cells 3-increased net loss
Loss of Potassium
Hypokalemia
Metabolic alkalosis
Diagnosis
• Diuretic and laxative abuse • Surreptitious vomiting • Marked leukocytosis(AML)
Pseudohypokalemia • TTKG
Treatment
• Correct K⁺ deficit and minimize losses • In intracellular shifts use oral
preparations. • In DKA there may be an underestimation of the K⁺ deficit. • Use
KCl and rarely Bicarbonate formulas.
Hyperkalemia
• Definition: plasma K⁺ concentration > 5 mmol/L • Causes: 1-Decreased renal
loss 2- increased potassium release from the cells. Pseudohyperkalemia:
PROLONGED use of a tourniquet-hemolysis-marked leukocytosis and
thrombocytosis.
Clinical features
• Weakness,flaccid paralysis and respiratory arrest • Metabolic acidosis • Cardiac
toxicity ECG changes: 1-increased T wave amplitude or tented T wave 2-
increased PR interval and widening of QRS 3-loss of P wave
ECG
Diagnosis
• • • • Exclude pseudohyperkalemia Symptoms Plasma K ECG
Treatment
• Depends on Plasma K conc +ECG changes+associated muscular weakness • If
>7.5 severe and may be fatal so emergency treatment: 1-Administration of Ca
gluconate(rule of 10) dose may be repeated if no changes in ECG 2-insulin
+GLUCOSE 3-IV NaHCO3 (specifically in metabolic acidosis)
Removal of K⁺
• If renal function is adequate: Loop and thiazide diuretics • Na polystyrene
sulfonate(SPS) • If renal function is impaired :Hemodialysis
Calcium
• Normal calcium level:8.9-10.1 g/dl • Regulation by PT glands+VitD • Regulating
diverse physiological processes
Hypercalcemia
• Causes: 1- Excess PTH 2-FHH (CaSR mutations) 3-PTHrP 4-Sarcoidosis 5-
Hyperthyroidism 6-Osteolytic metastasis
Clinical manifestations
• If mild asymptomatic however be careful of neuropshychiatric changes. • PUD •
Nephrolithiasis • If severe >12-13 mg/dl lethargy stupor or coma+GIT symptoms •
ECG changes:AV block-bradycardiashort QT interval
Diagnosis
• Note the albumin concentration 50% ionized-50% bound to albumin If there is
hypoalbuminemia add 0.8mg/dl for every 1g/dl albumin decrement and opposite
for increase in albumin • PTH level • Renal function
Treatment
• In severe hypercalcemia : 1-Hydration 4-6 L IV saline in 24 hours 2-Loop
diuretics 3-Bisphosphonates 4-Calcitonin 5-Dialysis 6-IV phosphate
Hypocalcemia
• PTH levels:
Clinical manifestaions
• Paresthesias:finger,toes,circumoral regions • Carpopedal spasm • Chvostek
sign • Trousseau sign • QT prolongation