Chapter 8 Flashcards
hydrostatic pressure
due to fluid volume, greater the fluid volume in a compartment the greater the hydrostatic pressure
osmotic pressue
due to the number of dissolved particles in solution (electrolytes and proteins).
- the greater the number of dissolved particles the greater the osmotic pressure
colloid osmotic pressure
osmotic pressure due to proteins
isotonic solutiom
no net movement of water
hypotonic solution
water moves in the cell - cell swells
hypertonic solution
water moves out of cell - cell shrinks
transudative edema
increased hydrostatic pressure/low oncotic pressure; high in fluid, low in protein (heart failure, nephrotic syndrome, cirrhosis)
exudative
inflammation; high in fluid and protein
Causes for transudative edema:
- Increased capillary pressure
- Decreased osmotic/oncotic pressure
- Lymphatic obstruction
Causes for exudative edema:
Increased capillary permeability
hormones that regulate water balance
- ADH
- Aldosterone
- ANP
- Renin Angiotensin system
ADH (antidiuretic)
increases water reabsorption by kidney (against urination)
aldosterone
tells the kidney to hold on to sodium and excrete potassium
ANP (atrial naturetic peptide)
increases the amount of sodium and water the kidney excretes, natriuresis and diuresis
Neurogenic diabetes insipidus
No ADH
Nephrogenc diabetes insipidus
No receptors for ADH
syndrome of inappropriate ADH (SIADH)
too much ADH - holding on to too much fluid - high blood volume
causes of hypovalemia
- Diarrhea
- Vomiting
- Excessive sweating
- Excessive urine loss
- GI suction
s/s of hypovolemia
- Increased thirst
- Weak pulse
- Increased heart rate
- Decreased blood pressure
- Decreased urine output
- Decreased skin turgor
- Increased hematocrit
- Dry mucous membranes
- Sunken eyes
treatment of hypovolemia
Fluid replacement
what causes hypervolemia
- Increased sodium followed by increased water
- Renal failure
- Heart failure
- Liver failure
S/S of hypervolemia
- Weight gain
- Edema
- Distended neck veins
- Bound pulse, increased BP
- Decreased hematocrit
treatment of hypervolemia
- sodium restriction
- diuretics
potassium wasting diuretics
- lasix
- hydrochlorothiazide
what electrolyte imbalance do potassium wasting diuretics cause
- low potassium
potassium sparing diuretics
- aldactone
- spironolactone
what electrolyte imbalance does potassium sparing diuretics cause
- high potassium
normal level of sodium
135 - 145 mEq/L
hyponaturemia level
<135 mEq/L
- fluid shift from ICF – ECF
- hypotonic
hypernatremia level
> 145 mEq/L
- water deficit
- Na+ administration
causes of Hyponatremia
- Excessive sweating
- Diarrhea
- Certain diuretics
- Insufficient aldosterone
- Decreased renal function/failure
- Excessive ADH secretion – - SIADH
- Excessive water intake
- Diluting baby formula
S/S of hyponatremia
- Muscle cramps
- fatigue/weakness
- Nausea/vomiting
- Decreased osmotic pressure – cell shift – cell swelling
- Confusion
- Seizures
- headache/lethargy
treatment of hyponatremia
- Limiting water intake
- Discontinuing medication
- Adminstration of IV saline
- Hypertonic saline with a diuretic
Hypernatremia causes
- Insufficient ADH
- lost of thirst mechanism/inability to communicate (dehydration)
- watery diarrhea
- excessive aldosterone
- impaired ability of kidney to conserve water
- high osmotic tube feeding w/o sufficient water
S/S Hypernatremia
- Increased thirst increased
- ADH secretion (expect if caused by lack of ADH
- Dry skin and mucous membranes
- Decreased skin turgor
- Decreased salivation
- Difficulty swallowing
- Confusion
treatment of hypernatremia
- Treat underlying cause
- If the underlying cause is diuretics: stop.
- If it is that their body are not responding to ADH: stop giving ADH
- Fluid replacement: if due to fluid loss
Potassium normal levels
3.5 to 5.0 mEq/L
hypokalemia causes
- Inadequate intake
- Diuresis associated with certain diuretics (lasix and hydrochlorothiazide)
- Excessive aldosterone
- Treatment of diabetic ketoacidosis with insulin (increase intracellular shift)
- Beta2 adrenergic agonists (intracellular shift)
- Metabolic alkalosis (excessive loss)
S/S hypokalemia
- Muscle weakness
- Fatigue/weakness
- Paresthesia (tingling of fingers)
- Cardiac arrhythmias
- Decrease ability of excitable cells to develop an AP (action potential)
causes hyperkalemia
- Renal failure (Kidneys job to get rid of excessive potassium)
- Decreased aldosterone
- Potassium sparing diuretics
- Prolonged acidosis (Potassium shifts out of the cells)
- Tissue injury (More potassium inside the cell then out)
- Rapid rate of administration of K+ (If you administer potassium too
S/S hyperkalemia
- Impaired neuromuscular function:
- Excitable cells do not repolarize
- Cardiac arrhythmias
- Muscle weakness
- Paresthesia
- Increase the ability to excitable cells (hyperreflexia) to develop an AP (action potential)
normal calcium levels
8.5 to 10.5 mg/dL
Hypocalcemia causes
- Hypoparathyroidism (PTH = Increases the parathyroid hormone, meaning you are not absorbing it)
- Malabsorption
- Vitamin D deficiency/resistance
- Elevated serum phosphate
- Increased serum pH (alkalosis): increased binding of calcium to protein
- Renal failure
- Increased urinary loss
S/S hypocalcemia
- Increased excitability of nerve
- Hyperactive reflexes
- Weak heart rate contractions
- Cardiac arrhythmias
- Blood pressure drops
causes of hypercalcemia
- Hyperparathyroidism
- Increased intake of vitamin D or excess dietary calcium
- Malignant bone tumors
- Bronchogenic tumors = secrete PTH
- Demineralization of bone due to immobility or bone tumors
- Acidosis
S/S hypercalcemia
- Hyporeflexia: depressed neuromuscular activity
- Loss of muscle tone
- Polyuria due to decreased function of ADH in kidneys
- Cardiac contraction increases in strength
- Bone pain
- Renal stones
normal phosphorus levels
2.5 - 4.5 mg/dL
causes of hypophosphatemia
- Malabsorption
- Excessive use of antacids
- Hyperparathyroidism
- Prolonged hyperventilation
- Refeeding syndrome
S/S hypophosphatemia
- Blood cells function less effectively
- Increased bleeding
- Impaired neurological function
- Tremors
- Confusion
- Paresthesias
- Dysphagia
- Anorexia
- Hyporeflexia
causes of hyperphosphatemia
renal failure
S/S
- Blood cells function less effectively
- Increased bleeding
- Impaired neurological function
- Tremors
- Confusion
- Paresthesias
- Dysphagia
- Anorexia
- Hyporeflexia
Normal level of magnesium
1.3 - 2.1 mEq/L
causes of hypomagnesemia
- Limited intake and excessive loss (intestinal or renal), shifting between compartments
- Malnutrition
- Starvation
- Prolonged nasogastric suctioning
- Decreased absorption
- Diarrhea
- Diabetes ketoacidosis = increased renal loss
- Hyperparathyroidism = increased renal loss
- Loop diuretics = increased renal loss
- Insulin = Shifts Mg into cells
causes of hypermagnesemia
- Renal insufficiency
- Magnesium containing medications including laxatives, antacids
S/S hypomagnesemia
- Hyperreflexia = increases activity of neuromuscular junction = hyperactive deep tendon reflexes
- Paresthesia
- Positive Chvostek or Trousseau signs
- Muscle twitching
- ECG changes
S/S of hypermagnesemia
- Decrease PTH secretion
- Decrease neuromuscular junction activity = muscle weakness = hyporeflexia
- Blocks calcium channel = effect on heart
- Decreased BP
what are electrolyte imbalances from hyperaldosteronism
- hypokalemia
- hypernatremia
S/S hyperaldosteronism
- Muscle weakness
- Cramps
- Paresthesia
- Hypertension
- Cardiac arrhythmias
- Palpitations
- Polyuria
- Polydipsia
- Nocturia
- Fatigue
- Headache
what are electrolyte imbalances of hypoaldosteronism
- hyperkalemia
- hyponatremia
S/S of hypoaldosteronism
- Muscle weakness
- Fatigue
- Hypotension
- Dizziness
- Cardiac arrhythmias
- Dehydration
- Nausea
- Confusion
Why do cancer patients treated with chemotherapy develop leukopenia
chemotherapy targets rapidly dividing cells, including both cancerous and healthy cells. Since bone marrow stem cells, which produce white blood cells (WBCs), are among the fastest-dividing cells in the body, they are highly susceptible to chemotherapy’s effects. As a result, WBC production decreases, leading to leukopenia.
Consequences of Leukopenia:
- increased infection risk
- delayed heaing
- fever and sepsis
- treatment interruptions
What is the physiological active form of calcium
ionized calcium
What happened to the physiological active form of calcium during acidosis and
Why?
Acidosis (Low pH, High H⁺) → More Ionized Calcium (↑ Ca²⁺)
Why?
Extra H⁺ binds to albumin, kicking calcium off, so more free Ca²⁺ is available.
What happened to the physiological active form of calcium during alkalosis and
Why?
Alkalosis (High pH, Low H⁺) → Less Ionized Calcium (↓ Ca²⁺)
Why?
Less H⁺ means more calcium binds to albumin, so less free Ca²⁺ is available.
Name all the electrolyte imbalances you would expect to see in a patient suffering from
kidney failure.
- low Na
- high K
- low Ca
- high PO4
- high Mg
- high H
What happens to potassium in acidosis
Acidosis (Low pH, More H⁺) → High K⁺ in Blood (Hyperkalemia)
H⁺ moves into cells, pushing K⁺ out into the blood.
