Alteration of Fluids in Cellular Environment

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Fluid And Electrolyte Imbalances

What Causes Fluid and Electrolyte Imbalance - e.g. Edema?
Maintenance of Intra and Extra-Cellular Fluids (ICF & ECF):

Water Movement Between ICF and ECF
• The movement between ICF and ECF is primarily a function of osmotic forces.
• Water moves freely by diffusion through the lipid bilayer, and through aquaporins. Aquaporins are water channel proteins that provide permeability to water.
• NA+ is the most abundant ECF ion, and is responsible for osmotic balance of the ECF.
• K+ maintains the osmotic balance of the ICF space.
• Osmotic force of ICF proteins and other non-diffusible substances is balanced by the active transport of ions out of the cell.
• The ICF is usually not subject to rapid changes in osmolality, but when there are changes in ECF osmolality, a net transfer of water from one compartment to another occurs until osmotic equilibrium is reestablished.

What Causes Fluid and Electrolyte Imbalance - e.g. Edema? Cont'd

Edema: is the excessive accumulation of fluid within the interstitial space. It is a problem of fluid distribution and does not indicate fluid excess. The pathologic process is an increase in the forces of fluid filtration from capillaries or lymphatic channels into the tissues.
The Mechanism of Edema:
1. Increased capillary hydrostatic pressure leads to
-Venous obstruction, Na+ and H2O retention, heart, renal failure causing edema

What Causes Fluid and Electrolyte Imbalance - e.g. Edema? Cont'd

2. Decreased plasma oncotic pressure
-Decreased production of plasma proteins (cirrhosis, malnutrition, Kidney)
3. Increased capillary permeability
-Loss of plasma proteins (burns, acute inflammation, immune response). Protein escapes plasma and produces edema and gain interstitial fluid proteins
4. Lymph obstruction
-Decreased absorption of interstitial fluid d/t blocked lymphatic channel (infection, Tumor, surgery) protein and excessive fluid build up in interstitial space (Lymphedema)

Abnormalities of Volume, Osmolality, Composition

Physiologic regulation of volume - 3 systems involved:
• Cardiovascular: ↓ CO2 → ↓ BP → baroreceptors → ↑ sympathetic NS → vasoconstriction & ↑ HR
• Renal: ↓ renal perfusion → baroreceptors → ↑ renin (renal)- angiotensin-aldosterone (adrenal cortex) system → ↑ renal Na+ reabsorption & systemic vasoconstriction
• Pituitary: ADH (antidiuretic hormone) may be released in conditions of extreme hypovolemia (5-10% loss of ECF)

I. Volume Imbalances: Hypovolemia (isotonic volume depletion)

o ECF volume deficit, ICF H2O increase
o GI losses, hemorrhage, severe wound drainage, decreased fluid intake, diaphoresis, third-spacing

Volume Imbalances Cont'd: Hypervolemia (isotonic volume excess) water excess

o ECF volume excess
o Renal disease/renal failure (renal Na+ retention), excessive IV NS (normal saline),
• As excessive ECF accumulates intravascular, shifts into interstitial compartment, causing edema due to high capillary hydrostatic pressure, pulmonary edema and ascites

II. Osmolality Imbalances: Cont'd Abnormalities

• Imbalances in the concentrations of solutes/ions in body water (tonicity)
• Causes a change in osmolality (osmotic concentration-ionic concentration per unit of solution) and measurement
• Because Na+ is the most active osmole in ECF, osmolality is usually closely related to the concentration of Na+
• Exceptions include hyperglycemia, uremia, or hyperosmolar states resulting in osmotic diureses
• Loss or deficit of free water such as in dehydration

III. Hypo-osmolality - (Hypotonicity ≈ Hyponatremia) Cont'd Abnormalities

• ECF is more dilute than ICF < 0.9
• Free water excess (H2O Intoxication & both ECF & ICF volume Increases)
• Hyponatremia - depletion - not enough Na+ to hold H2O in ECF
• Decreased ECF volume
• Cellular swelling or edema (water moves into the cell - osmotic pressure greater) and causes Cerebral and Pulmonary Edema
• Plasma Volume Decreases (Hypovolemia)

IV. Hyper-osmolality - (Hypertonicity ≈ Hypernatremia) Cont'd Abnormalities

• ECF is more concentrated than ICF > 0.9
Causes of concentrated ECF:
• Water deficit / loss of free water; gain solute (Hypovolemia)
• Increased ECF volume (Hypervolemia)
• Hypernatremia Na+ holds on to H2O in ECF& increase ECF volume
Consequences of concentrated ECF:
• Cell shrinkage & dehydration, tachycardia, weak pulses
• Cerebral neuron shrinkage, thirst, fever, confusion, coma

What does ADH (Anti-Diuretic Hormone) do and where does it come from?

Antidiuretic Hormone (ADH):
• Activates osmoreceptors (In Hypothalamus)
• ADH controls the final concentration of urine.
• Secreted by the Hypothalamus-pituitary renal system & neurohypophysis.
• Increases water permeability in the last segment of the distal tubule and along the entire length of the collecting ducts (H2O returns from Urine)
• Released in extreme thirst causing Hypovolemia (5-10% of ECF loss)

In the presence of ADH: Cont'd

• Impaired or decrease ADH secretion or function leads to excessive H2O loss and causing Diabetes Insipidous (DI)

In the absence of ADH or Increased ADH Release: Cont'd

• Syndrome of Inappropriate ADH release (SIADH) - inappropriate stimulation of ADH secretion

The Role of Potassium, Sodium, and Calcium both inside and outside the Cell: Hyper/Hypo

Potassium (K+):
-- Imbalances are relatively common and potentially life threatening.
-- ICF: ECF 155mEq/l: 4mEq/l
* K+ gradient maintained by Na+/K+ pump
* Gradient results in resting membrane potential in excitable tissue
• Extracellular Fluid:
o Primary role -modulate neuromuscular conduction (particularly in cardiac conduction)
• Intracellular Fluid:
o Primary role-maintain intracellular volume

Physiologic Regulation of K+

Relatively passive; renal excretion continues even without intake.
• Aldosterone
o Released as part of rennin-angiotensin-aldosterone system in response to decrease renal flow→ ↑ renal Na+ reabsorption
o To reabsorb the Na+, K+ is secreted in the urine
• pH of ECF (typical metabolic acid-base disorders)
o Acidosis K+ → ECF
o Alkalosis K+ → ICF
o For every 0.1 unit fall in pH, serum K+ increases by 0.5 mEq/l
•Circulating hormones/ligands
o ↑ insulin, K+ →ICF
o ↑ Epinephrine, K+ → ICF
o ↑ Alpha-adrenergic agonists, K+ → ECF

Imbalances of K+

Consequences: Nausea/vomiting; neuromuscular weakness, hypotonicity, parathesia; cardiac dysrhythmias

• Hypokalemia K + <3.5 mEq/l

• GI, urinary (diuretic-induced) losses; inadequate K+ intake; metabolic alkalosis; hyperinsulinemia
• K+ effect on nerve & muscle
• ICF even more negative compared to ECF
• Hyperpolarized-less likely to fire

• Hyperkalemia K+ >5.5 mEq/l

• r/o psuedohyperkalemia (RBC Lysis releases K+ → ECF)
• Inadequate K+ excretion (renal failure, hypoaldosteronism, K+ sparing diuretics); metabolic acidosis; extensive tissue damage; excessive K+ intake.
• K+ effect on nerve & muscle
• ICF less negative compared to ECF
• Slightly depolarized-more likely to fire

Sodium (Na+)

- Sodium regulates extracellular osmotic forces and therefore regulates water balance

Hyponatremia Na+ < 135mEq/l

o Inadequate intake, hypoaldosteronism, excessive diuretic therapy- Furosemide, Ethacrinic acid, Thiazides
o ECF effects-extracellular volume contraction and hypovolemia (but may not be if there is water excess)
o ICF effects- increased intracellular water; edema; brain cell swelling, irritability, depression, confusion; systemic cellular edema, including weakness, anorexia, nausea and diarrhea

Hypernatremia Na+ > 147mEq/l

o Excessive hypertonic salt solutions- IV hypertonic sodium, saline-induced abortions, selected infant formulas; hyperaldosteronism; Cushing syndrome
o ECF effects- Hypervolemia- weight gain, bounding pulse, increased BP, edema, venous distention; neuromuscular symptoms- muscle weakness, seizures
o ICF effects- Intracellular dehydration-thirst, fever, decreased urine output, shrinkage of brain cells-confusion, coma, cerebral hemorrhage

Calcium (Ca+)

Imbalances - relatively rare but potentially life threatening
• Only the ionized (free) form are biologically active
o Inactive in bound to plasma proteins (i.e. ECF Ca++) or ATP (i.e. ICF Mg++)
• Significantly stored in bone/teeth
o 99-100% of Ca++ and PO4
o 40-50% of Mg++
• All are in low and carefully regulated concentrations in the ECF
o Ca++ ECF > ICF
o PO4 and Mg++ ECF < ICF
o Ca++ inversely proportional to PO4

• Wide ranging intracellular and extracellular roles. Ca+ Cont'd

o Ca+ - excitability and permeability of cell membranes, neurotransmitter release, muscle excitation and contraction, act as a second messenger
o PO4 - part of phospholipids; protein phosphorylation; acts as a urinary buffer to maintain acid-base balance
o Mg++ - required to activate many enzymes/enzyme systems; required for protein synthesis; determine receptor sensitivity

Physiologic Regulation of Calcium (Ca+)

• Controlled by
o Parathyroid hormone (PTH)
o Calcitonin (activated vitamin D)
• Act on three sites
o Gut (dietary absorption)
o Bone (release from/add to stores)
o Kidney (renal excretion)

Calcium Homeostasis

• 99% of body calcium in bones
• 1% ECF (serum); critical to life processes
• Ca++ is drawn from bones when Ca++ intake is inadequate
• Homeostasis via parathyroid hormone (PTH) and 1,25-dihydroxyvitamin D (calcitriol)

Imbalances of Calcium: Hypocalcemia Ca ++ < 4.5 mEq/l

o Caused by a PTH or activated vitamin D deficiency, blood administration, inadequate GI absorption of calcium, inadequate intake of calcium
o Symptoms- increased neuromuscular irritability (calcium is a neurotransmitter in the junction between the nerve and muscle), tetany; diarrhea, osteoporosis (long-term)
o Ca++ effect on nerve & muscle
• Threshold potential is closer to membrane potential, thus cell more likely to fire
o Hormone regulation by PTH
• ↑ PTH → ↑ renal activation of vitamin D → ↑ interstitial absorption of calcium; ↑ renal reabsorption of Ca++ and ↑ excretion of PO4; ↑ bone reabsorption of Ca++

Imbalances of Calcium: Hypercalcemia Ca ++ > 5.5 mEq/l

o Causes included hyperparathyroidism; bone metastasis with bone reabsorption, Ca++ producing tumors
o Symptoms- muscular weakness, decreased tone; constipation
o Effect on nerve & muscle
• Threshold potential is further from membrane potential, thus cell less likely to fire
o Hormone regulation by PTH
• ↓ PTH → ↓ renal activation of vitamin D → ↓ interstitial absorption of calcium; ↓ renal reabsorption of Ca++ and ↓ excretion of PO4; ↓ bone reabsorption of Ca++

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