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55 Cards in this Set

  • Front
  • Back
Osmolality is determined by what?
Determined by sodium and its anions, chloride & bicarbonate
Isotonic Soulution
•ECF & ICF has same osmolality
•No concentration gradient
•No fluid shift across cell membrane
Hypotonic Solution
•ECF has lower osmolality than ICF
•Concentration gradient
•Fluid shifts from ECF to ICF (Cells Swell)
Hypertonic Solution
•ECF has greater osmolality than ICF
•Concentration gradient
•Fluid shifts from ICF to ECF (Cells Shrink)
•Fluid shifts from vascular compartment to the interstitial compartment
•Swelling noticeable when interstitial volume expands by 2.5 - 3.0 Liters;
•1 Liter=2.2 lbs.
Causes of Edema
1. Increased Capillary Hydrostatic Pressure
•Increased Vascular Volume
•Venous Obstruction
2. Decreased Colloid Osmotic Pressure
•Increased Loss of Plasma Proteins
•Decreased Production of Plasma Proteins
3. Increased Capillary Permeability
•Allergic Reaction
•Tissue Injury & Burns
4. Obstruction of Lymphatic Flow
•Produces lymphedema
Effects of Edema
increased distance for diffusion of O2, nutrients & wastes
•Edematous tissue more susceptible to tissue damage
Sodium Function
Regulates ECF Fluid Volume,
Regulates Acid-Base Balance
(•Na+ combines with bicarb (HCO3)),Facilitates impulse transmission in muscle/nerve fibers
Sodium Regulation
major regulator
•Responds to changes in arterial pressure & blood volume by adjusting glomerular filtration and rate at which Na+ is filtered from the blood
Sodium Gains/Losses
Gains: diet
Losses: Kidney, GI, and Skin
Water Gains/Losses
Gain: 2500cc (food/fluid)
Loss: 2500cc (urine, stool, skin, lungs)
Sensible Losses (water)
Aware of Losses
Insensible Losses (water)
Unaware of losses
Obligatory UO
•Thirst center in hypothalamus
•Thirst stimulated when blood volume ↓ OR ECF osmolality ↑
•Andidiuretic Hormone or Vasopressin
•Released in response to ↓ in blood volume of ↑ in ECF osmolality
•Acts on kidneys to reabsorb water
•↑ ADH = ↑ reabsorption of water = ↓ UO
•↓ ADH = ↓ reabsorption of water = ↓ UO
•Proportionate losses of Na+ & Water
•Losses are isotonic
•Contraction of ECF (Interstitial & vascular)
•No change in osmolality, No Fluid Shift
Causes of Hypovolemia
V, D, DM (blood sugar↑), Lasix (diuretic), Polyuria, ↓Aldosterone (addisons disease or Adrenal Insufficency),
S/S of Hypovolemia
Weight Loss, Thirst, Dry Mucous Membranes, Poor Skin Turgor, Increased capillary refill time, Decreased BP, Postural (orthostatic) Hypotension, Weak, rapid pulse, Decreased UO (except in osmotic diuresis), Increased Hematocrit (hemoconcentration)
•Proportionate gain in sodium & water
•Losses are isotonic
•Expansion of ECF (interstitial & vascular)
•No change in osmolality, No Fluid Shift
Causes of Hypervolemia
↑ Sodium & Water Retention due to: CHF, Renal Failure (Decreased UO), Liver Failure(Increased Aldosterone),
Cushing’s Disease (Increased Cortisol)
S/S Hypervolemia
Weight gain, Edema, Increased BP, Full, bounding pulse, JVD (jugular venous distention), Pulmonary Edema, SOB / Dyspnea, Crackles, Cough, Increased UO
< 135 mEq/L Na+
•Sodium Loss or Water Gain
•Water Gain = More common form (Dilutional Hyponatremia)
•ECF Hypotonic (Decreased serum osmolality)
•Fluid Shift from ECF to ICF (Cells Swell)
Causes of Hyponatremia
water gain due to
• Psychogenic Polydipsia
• Compulsive water drinking
•SIADH (Syndrome of Inappropriate ADH secretion)
•↑ ADH + ↑ reabsorption of water = ↓ UO
•Using tap water to replace Na+ losses during heavy exercise or V&D
S/S Hyponatremia
Serum Osmol.< 275 mOs/kg of H20, ECF to ICF (Cells swell), Abdominal Pain, A, N, V, D, Increased UO (except in SIADH ↓ UO), Muscle cramps, Muscle Twitching, Fatigue, Weakness, Lethargy, Confused , Disoriented, ↓ DTR, Seizures, Coma
> 145 mEq/L Na+
Sodium Gain or Water Loss
Water Loss - More Common (Dehydration)
ECF = Hypertonic (osmolality > 295)
Fluid Shift = ICF to ECF (cells shrink)
Causes of Hypernatremia
Sodium Gain:
•Rapid infusion of Na+ containing IV
Decreased Water Intake
•Unavailability of water
•Unable to swallow due to oral trauma
•Impaired thirst sensation
•Inability to express thirst
Water Loss
•Diabetes Insipidus
- ↓ ADH = ↓ Reabsorp. of Water =↑ UO
•Severe Watery Diarrhea
S/S Hypernatremia
Serum Osmol.> 295 mOs/Kg of H20, ICF to ECF (cells shrink), Thirst, Dry Mucous Membranes, Poor Skin Turgor, Decreased BP, Tachycardia, Weak Pulse, Oliguria (except in Diabetes Insipidus), Restless, Agitated, Confused, ↑ DTR,Seizures,Coma
Potassium Function
Regulates ICF Volume(Major ICF Cation)
Regulates Acid-Base Balance
•Exchange between H+ & K+
Facilitates Impulse Transmission in Nerve & Muscle fibers
•Na+ & K+ transported across cell membrane
•Causes cell membrane depolarization
•Creates an action potential
•Generates nerve/muscle activity
•Affects skeletal, smooth & cardiac muscle
Potassium Regulation
Kidneys: Retain/Excrete, Aldosterone:
•↑ Aldosterone ↑ Na+ & Water ↓ K+
•↓ Aldosterone  ↓ Na+ & Water ↑ K+
Exchange Between K+ & H+:
•Acidosis (↓ pH) = H+ moves into ICF K+ moves in ECF
•Alkalosis (↑ pH) = H+ moves into ECF K+ moves into ICF
Potassium Gains/ Losses
•Diet = Need 10-30 mEq/day
•Found in variety of fruits & vegies
•Kidneys = excrete 80-90% of K+ in urine
•GI & Skin = Approx. 10-20% lost in stool & sweat
< 3.5mEq/L K+
Causes of Hypokalemia
Decreased Intake
•Anorexia, Fasting
•NPO - Fail to replace losses especially after surgery
•Diuretics (Lasix)
↑ Aldosterone
•Na+ & Water are reabsorbed; K+ excreted
•Excessive ingestion of black licorice
↑ Cortisol
•Cushing’s Syndrome
•Na+ & Water are reabsorbed; K+ excreted
GI Losses
•V, D, Laxative abuse
•Compensatory response to fluid loss = ↑ Aldosterone
Shift of K+ from ECF to ICF
•Alkalosis (↑ pH)
•Excess Insulin
•Excess beta adrenergic stimulation
S/S Hypokalemia
Affects skeletal, smooth & cardiac muscle, Cells become hyperpolarized, Moves resting membrane potential (RMP) away from threshold, Makes it more difficulty to achieve action potential, ↓ Nerve/Muscle Activity, Bradycardia, Weak, irregular pulse, Postural (orthostatic) hypotension, ECG Changes, Cardiac Dysrhythmias, Cardiac Arrest, ↓ Peristalsis= Paralytic Ileus (severe hypokalemia), ↓ Bowel Sounds, Abdominal Distention, A, N, V, Constipation, Polyuria (interferes with the action of ADH at the renal tubules), ↓ Specific Gravity, Thirst, Fatigue, Paresthesia, Muscle Weakness, Muscle Cramps (esp. with exercise), Paralysis (severe hypokalemia)
> 5.0 MEQ/L K+
Causes of Hyperkalemia
Excessive K Intake
•Dietary excess uncommon as long as kidneys function
•Excess IV replacement
Renal Failure
•Oliguria / Anuria
↓ Aldosterone
•Addison’s Disease
•↓ Na+ & Water & ↑ K+
•Potassium-Sparing Diuretics
•ACE Inhibitors (Angiotensin Converting Enzyme)
Shift from ICF to ECF
•Tissue Injury that causes cell death - Crushing or Burn injury -
•Strenuous Exercise
•Metabolic Acidosis (↓ pH)
S/S Hyperkalemia
Affects skeletal, smooth & cardiac muscle, Cells become hypopolarized, Moves resting membrane potential (RMP) closer to threshold, Makes it easier to achieve action potential, ↑ Nerve/Muscle Activity, ECG Changes, Arrhythmias, Cardiac Arrest, ↑ Peristalsis, ↑ Bowel Sounds, Abdominal Cramps, N, V, D, Paresthesia (1st symptoms), Muscle Cramps, Muscle weakness (esp. lower extremities), Flaccid Paralysis?
Ionized Calcium
•Free Calcium
•Carries out physiologic function
Protein-bound calcium
•Calcium bound to primarily to albumin
Complexed Calcium
•Calcium bound to anions - citrate, phosphate, sulfate, carbonate
Calcium Function
Bones & Teeth (99%)
•Provides strength & stability
Cell Membrane Permeability
•↓ Ca++ = allows Na+ to enter cell= ↑ Nerve/Muscle Activity
•↑ Ca++ = blocks Na+ from enter cell = ↓ Nerve/Muscle Activity
Blood Clotting
Acid-Base Balance
Calcium Regulation
Parathyroid Hormone (PTH)
•Releases Ca++ from bone
•Increases kidney reabsorption of Ca++
•Helps activate Vitamin D to active form to ↑ GI absorption
Vitamin D
•Inverse relationship between Ca++ & PO4
Serum pH
•Inverse relationship between Ca++ & pH
•Produced by thyroid gland
•Inhibits bone resorption of Ca++
Vitamin D
•Classified as vitamin; functions like hormone
•Precursor of active form of vitamin D obtained from diet OR synthesized by skin when exposed to sunlight
•Liver & Kidney metabolize Vitamin D to active form CALCITROL
•Active form of Vitamin D + PTH work together to increase GI absorption of Ca++
Active form of Vitamin D
Ca++ Gains/Losses
Gains: diet, need 1000 to 1500mg/day
Losses: Urine (Kidneys),
Stool (GI)
People at risk for inadequate Ca++ intake
•Poor diet, poor absorption
Menopausal Women
•↓estrogen, moves calcium out of bone
•Inadequate intake of calcium, poor absorption, sedentary
•Decreased weight bearing ca ++ pulled out of bone
Lack of Sunlight
•Vitamin D deficiency
<8.5 mg/dl
Hypocalcemia causes
↓ Calcium Intake or Absorption
•Diet with insufficient Ca++ & Vitamin D
•Excess dietary oxylates and phytates (peas beans legumes)
•Chronic Diarrhea (laxative abuse)
•Malabsorption Syndromes
↓ Physiologic Availability of Calcium
•↓ PTH (Hypoparathyroidism)
•↑ Phosphate (Renal Failure)
•↓ Magnesium (Inhibits PTH)
•Large transfusion of citrated blood
S/S Hypocalcemia
S/S related to ↑ neuromuscular irritability, Allows sodium to enter cell, Causes a decrease in threshold potential of excitable cells, Action potential is generated more easily, ↑ Nerve/Muscle Activity, Dental caries, Osteoporosis - Loss of bone mass; predisposed to pathologic fx, Hypotension, ↓ Cardiac Output, Dysrhythmias (heart block, ventricular fib), ECG Changes, Paresthesia, Muscle Twitching, Muscle Spasms, Hyperactive DTR’s, Tetany (Twitching, Spasms, Convulsions)
Tests to Assess Tetany
Chvostek (vos’teks):
•Tap facial nerve in front of ear
•(+) = twitching of lips, nose & facial muscles

Trousseau Sign
•Apply BP cuff to upper arm
•Inflate 20 mm Hg above systolic pressure
•Applies pressure to nerves & blood vessels of upper arm
•(+) = spasm of hand & wrist
<10.5mg/dl Ca++
Causes of Hypercalcemia
↑ Ca++ intake or Absorption
•Milk-Alkali Syndrome = excess intake of milk and antacids
•Vitamin D Overdose
Shift of Ca++ from Bone to ECF
•↑ PTH (Hyperparathyroidism)
•Malignant Neoplasms
↓ Ca++ Excretion
•Thiazide Diuretics (prescribed for some menopausal women)
•Lithium (bipolar)
↓ pH (acidosis)
•↓ binding of Ca++ with protein
•↑ Ionized Ca++
S/S of Hypercalcemia
S/S related to ↓ neuromuscular irritability, Blocks sodium from entering cell, Causes an elevation of the threshold potential of excitable cells, Takes more of a stimulus to generate an action potential, ↓ Nerve/Muscle Activity, Hypertension, Bradycardia, AV Block, Cardiac Arrest, Decreased GI Motility, A, N, V, C, KIDNEY STONES, Polyuria, Thirst, Fatigue, HA, Confusion, Personality Change, Muscle Weakness, Loss of Muscle Tone, Diminished Reflexes. Pathologic Fx = if hypercalcemia caused by bone resorption), Coma
Common causes of Lymphedema
Malignant obstruction
Surgical removal of lymph nodes