Exam 1: fluid, electrolyte imbalances Flashcards
e
what are the etiology of fluid volume deficit (hypovolemia)?
o water deprivation (confusing or coma, loss of thirst, inability to communicate)
o water loss (diarrhea, diabetes insipidus, excessive diuresis, hemorrhage, wound drainage, sweating)
Clinical manifestations of hypovolemia: (9)
o weight loss, weak pulses, tachycardia, thirst, decreased urine output, shrinkage of brain, increased hct, flattened neck veins, normal/decreased BP
what are the etiology of fluid volume excess (hypervolemia)?
o excessive pure water intake, excessive IV hypotonic solution administration, drinking water to replace isotonic fluid losses, tap water enemas, SIADH, renal water retention, hypersecretion of aldosterone
Clinical manifestations of hypervolemia: (7)
o edema, increased BP, bounding pulse, weight gain, venous distension, can develop into pulmonary edema, HF
what is a good indicator for dehydration?
- high Na=dehyration/fluid volume deficit (shortage)
etiology of hypernatremia
**serum sodium >145
o Excessive hypertonic solutions, hyperaldosteronism, cushing syndrome
o Hypovolemic (loss Na and water), euvolemic (loss of free water), or hypervolemic (increase body water and greater Na) depending of ECF water
Risk factors: age, mental state, fever, diarrhea, vomiting, DM, tube feedings, diuretics
clinical manifestation of hypernatremia
o CNS symptoms; weakness, lethargy, muscle twitching, hyperreflexia, confusion, coma
o intracellular dehydration
o Hyperchloremia, bicarb deficits (hyperchloremic metabolic acidosis)
treatment for hypernatremia
-oral fluids
-isotonic salt-free fluid
what is a good indicator for over hydration?
- hyponatremia
-serum sodium <135
-fluid overload!
etiology of hyponatremia:
o Vomiting, diarrhea, renal losses from diuretics, inadequate aldosterone secretion, SIADH, hypothyroidism, PNA, glucocorticoid deficiency, inadequate intake of Na, water intoxication, SSRIs, cirrhosis, HF
clinical manifestation of hyponatremia:
o Nausea/vomiting, headache confusion, lethargy, seizures, coma, hypotension, tachycardia, decreased urine output, weight gain, edema
o Less than 120= cell swelling
treatment of hyponatremia
-Water restriction
- hypertonic saline solution
-ADH receptors antagonist (vaptans)
what happens to potassium levels when there is tissue damage?
potassium levels rises b/c cell contents leaks out
what electrolyte levels should you monitor when urine output decreases?
potassium and mg
*these can only be excreted by the kidneys
etiology of hyperkalemia
serum K >5.0
o Excess dietary or IV K intake, renal failure, K sparing diuretics, hypoaldosteronism
o excessive intake, shift from ICF to ECF with change of cell permeability like from cell trauma,
o decreased renal excretion, use of stored whole blood, boluses of pcn G, K replacement, hypoxia, acidosis, insulin deficits, Digitalis overdose, renal failure, hypoaldosteronism, drugs that decrease renal K excretion
clinical manifestation of hyperkalemia
o muscle weakness, paralysis, dysrhythmias, increased neuromuscular irritability
o Dysrhythmias, (peaked T waves, prolonged PR, absent P wave, or widened QRS)
o anxiety, tingling, numbness
treatment of hyperkalemia
-EKG
- calcium gluc
-glucose
-insulin
-dialysis
etiology of hypokalemia
serum potassium <3.5
o Diarrhea, vomiting, starvation, inadequate replacement, K losing diuretics, hyperaldosteronism
o Most common cause; alkalosis!!!
o insulin admin, treatment of anemia with Vit B12 or folate, familial hypokalemic periodic paralysis (rare disease), DKA, GI/renal disorders, diuretics, hyperaldosteronism from adrenal adenoma, magnesium deficiency, some antibiotics
clinical manifestations of hypokalemia:
o Hypotension,
o ECG changes (flattened T waves, ST depression, peaked P wave, prolonged QT),
o V fib, cardiac arrest, lethargy, fatigue, muscle weakness
treatment of hypokalemia
-ekg
-K replacement
**concurrent with hypomagnesemia
etiology of hypercalcemia:
serum Ca >10.5
o Hyperparathyroidism, tumors, sarcoidosis, bone mets w/ calcium resorption, excessive vit D, prolonged immobilization, acidosis
clinical manifestations for hypercalcemia:
o Fatigue, weakness, lethargy, anorexia, nausea, constipation, mental status changes, impaired renal fx, kidney stones, EKG changes
treatment for hypercalcemia (4)
o Oral phosphate
o IV NS for renal secretion
o Calcitonin
o Denosumab
human monoclonal antibody for the treatment of osteoporosis, treatment-induced bone loss, metastases to bone, and giant cell tumor of bone.
o Treat underlying condition causing hypercal
etiology for hypocalcemia:
- Concentration levels <9, ionized levels <5.5
- Etiology:
o Nutritional deficiencies, inadequate intestinal absorption, decreased PTH, decreased vitamin D, deposition of ionized Ca into bone or soft tissue, removal of parathyroid glands, malabsorption of fat, bone mets, blood transfusions, pancreatitis, alkalosis, hypoalbuminemia
clinical manifestations for hypocalcemia
o Tingling, muscle spasms (particularly in hands and feet), cramping, hyperactive bowel sounds, fractures, tetany in severe cases
o Chvostek sign (tap face) and Trousseau sign (contraction of hand)
o convulsions, tetany, EKG changes
treatment for hypocalcemia
o IV calcium gluconate, PO calcium replacement
Pseudohyponatremia
o Hyponatremia with normal tonicity
o rare condition
o serum sodium is low but the serum osmolality and tonicity is normal or above normal;
o low Na concentration with normal osmolality may be an artifact due to the accumulation of other plasma constituents (triglycerides or proteins) in plasma
True hyponatremia:
o Hyponatremia with hypotonicity,
o most common form of hyponatremia**
o usually caused by impaired renal water excretion in the presence of continued water intake
Dilutional hyponatremia:
o Hyponatremia with hyperosmolality,
o usually d/t hyperglycemia
o the increase in glucose in ECF moves water from the cells to the ECF and dilutes Na concentration
o the Na concentration falls about 1.6 for every increase of 100 glucose
what is the definition of edema?
disproportionate amt of fluid in the interstitial space
what does oncotic pressure do?
it makes the movement of water into capillary greater than movement of water into interstitial compartment
what are usually the causes of edema? (5)
o 1) increased capillary venous hydrostatic pressure
o 2) decreased capillary oncotic pressure
o 3) lymphatic obstruction/dysfunction
o 4) increased capillary permeability
o 5) sodium and water retention.
what can increased capillary hydrostatic pressure result from? (2)
-venous obstruction
-sodium and water retention
how does venous obstruction affect hydrostatic pressure?
it causes hydrostatic pressure to increase behind the obstruction, pushing fluid from the capillaries into the interstitial spaces
what are common causes of venous obstructions? (5)
-venous blood clots
-hepatic obstructions
-right HF
-tight clothing around the extremities
-prolonged standing
what causes decreased plasma oncotic pressure?
losses or diminished production of plasma albumin
what happens when there is a decreased oncotic attraction fluid within the capillary?
it causes the fluid to move into the interstitial space, resulting in edema
what can liver disease or protein malnutrition cause?
decreased synthesis of plasma protein and decreased oncotic pressure
what can cause loss of plasma proteins? (3)
-glomerular diseases of the kidney (nephrotic syndrome)
-hemorrhage
-serous drainage from open wounds or burns.
what is increased capillary permeability usually associated with? (2)
-inflammation
-the immune response ( these responses are often the result of trauma such as burns or crushing injuries, neoplastic disease, allergic rxn, and infections)
why is edema caused by increased capillary permeability often very severe?
because of loss of proteins from the vascular space, which decreases capillary oncotic pressure and increases interstitial oncotic pressure with both processes facilitating fluid movement into the interstitial space.
classifications for: pitting edema
-few proteins in the fluid
-increased capillary venous hydrostatic pressure, decreased capillary oncotic pressure
classification for: non-pitting edema
-fluid has lots of protein in it
-increased capillary permeability, lymphatic obstruction
clinical manifestions of: metabolic acidosis (8)
- Headache
-lethargy
-confusion and coma later
-deep, rapid respirations (kussmaul)
-anorexia
-vomiting
-diarrhea
-dysrhythmias
clinical manifestions of: metabolic alkalosis (6)
-Weakness
-muscle cramps
-hyperactive reflexes
-respirations are slow
-confusion
-convulsions
what is contraction alkalosis
also known as hypochloremia metabolic alkalosis
occurs when acid loss is caused by vomiting or gastric suctioning with depletion of ECF sodium, chloride, and potassium
* This is loss of fluids from the body that are low in bicarb
examples of contraction alkalosis (3)
-diuretic therapy (thiazide/loop)
-vomiting
-GI suction
loss of hydrogen ions occurs d/t: extrarenal
usually results from GI losses or shift of hydrogen ions from EC to IC compartment
loss of hydrogen ions occurs d/t: renal
usually occurs d/t increase mineralocorticoid activity
(i.e. Hyperaldosteronism, Cushing’s, congenital adrenal hyperplasia, renal artery stenosis)
etiology of respiratory alkalosis
o alveolar hyperventilation, low CO2
o stimulation of ventilation is precipitated by hypoxemia.
o High altitudes
o Hypermetabolic states
o Fevers, anemia, thyrotoxicosis,
o Salicylate intoxication
o anxiety or panic attack disorder
o Improper use of mechanical ventilators can cause iatrogenic respiratory alkalosis.
o Secondary respiratory alkalosis may develop from hyperventilation stimulated by metabolic acidosis, causing a mixed acid-base disorder.
what is the normal anion gap
14-18
cation in ECF
most cations in the ECF are Na and a little potassium
anion in ECF
most anions in the ECF are Cl bicarb
if the metabolic acidosis is present and the gap is normal
we know that the cause is a loss of bicarbonate- usually from GI tract or kidneys, also known as “hyperchloremic metabolic acidosis”
* diarrhea (all secretions below stomach are rich in bicarb)
* renal tubular acidosis
o type 1 distal RTA
o type 2 proximal RTA
o type 4 hyperK RTA
all involve a defect in bicarb reabsorption and hydrogen ion excretion and are characterized by a + urinary anion gap
what causes elevated anion gap metabolic acidosis? (9)
**caused by the addition or retention of acid (usually results of renal defect)
o Paraldehyde,
o lactic acidosis,
o uremia,
o methanol,
o salicylates,
o ethanol,
o ethylene glycol,
o DKA,
o starvation
why is normal anion gap metabolic acidosis also referred to as hyperchloremic metabolic acidosis?
b/c when a bicarb is lost, more chloride is reabsorbed, keeping the gap normal
what are some causes of normal anion gap metabolic acidosis? (3)
-diarrhea
-laxative abuse
-drainage via fistulas, surgical drains, and urinary diversions
relationship among acidosis and alkalosis with: hydrogen
- as the H increases; pH decreases
-the greater the H; the more acidic
-the less the H; the more alkalotic
relationship among acidosis and alkalosis with: Calcium
-levels drop in alkalosis
-levels rise in acidosis
relationship among acidosis and alkalosis with: potassium
o K rises about 0.3 for each 0.1 decrease in pH in respiratory acidosis
o K rises about 0.7 for each 0.1 decrease in pH in metabolic acidosis
o K falls about 0.3 for each 0.1 increase in pH (alkalosis)
Low K is seen in metabolic alkalosis
High K is seen in metabolic acidosis
what is the relationship between Mg and Phos
-inversely proportional
-if one goes down, the other goes up
what are the causative factors of hypertonic imbalances? (3)
-increased sodium (hypernatremia)
-water deficit
-hyperglycemia
what are the causative factors for hypotonic imbalances? (6)
-decreased sodium (hyponatremia)
-water excess
-nephrotic syndrome
-cirrhosis
-HF
-isotonic dehydration treated with IV D5W (glucose in D5W solution is metabolized in water, contributing to hyponatremia)
What disease can cause hypotonic imbalances? (3)
-nephrotic syndrome
-cirrhosis
-HF
