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200 vocabulary-style flashcards covering fluid, electrolyte, and acid-base balance based on the provided lecture notes.
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Total body water percentage of a newborn baby
About 75% of their body weight
Total body water content of adults
60% men, 50% women
Reason women average less body water than men
They average more adipose tissue, which displaces water
Total body water volume in a 70 kg (150 lb) adult
42L
Body water percentage in obese and elderly people
45% by weight
Fluid compartments
Areas separated by selectively permeable membranes and differing in chemical composition
65%
Percentage of body water in intracellular fluid
Percentage of body water in extracellular fluid (ECF)
35%
Subdivision of ECF: Tissue (interstitial) fluid
25%
Subdivision of ECF: Blood plasma and lymph
8%
Subdivision of ECF: Transcellular fluid
2%
Examples of transcellular fluid
CSF, synovial, peritoneal, pleural, and pericardial fluids; vitreous and aqueous humors; digestive, urinary, and reproductive tract fluids
ICF vs. ECF osmolarity relationship
They are equal because water moves easily through membranes
Osmotic gradients duration
They never last long because osmosis restores balance within seconds
Primary electrolytes in ECF
Sodium (Na+) salts
Primary electrolytes in ICF
Potassium (K+) salts
Principals governing body water distribution
Electrolytes
Fluid balance
Condition when daily water gains and losses are equal, approximately 2,500mL/day
Metabolic water
Water formed by aerobic metabolism and dehydration synthesis
Preformed water
Water ingested in food and drink
Routes of water loss
Urine, feces, expired breath, sweat, and cutaneous transpiration
Cutaneous transpiration
Water that diffuses through the epidermis and evaporates
Insensible water loss
Output of which one is not usually aware, including expired breath and cutaneous transpiration
Sensible water loss
Noticeable output, including urine and moderate sweating
Obligatory water loss
Output that is unavoidable, such as in expired air and feces
Primary regulator of fluid intake
Sense of thirst
Conditions leading to thirst
Dehydration reducing blood volume and pressure, and increasing blood osmolarity
Osmoreceptors
Sensors that respond to angiotensin II and rising osmolarity of ECF
ADH (Antidiuretic Hormone) source and thirst role
Released by the hypothalamus to promote water conservation and stimulate the cortex for thirst
Long-term inhibition of thirst
Absorption of water from the small intestine reduces blood osmolarity
Short-term inhibition of thirst
Distension of the stomach and intestines by ingested water
Regulation of water output
Primarily achieved through variation in urine volume
Kidney limitation in fluid balance
Cannot replace water or electrolytes; can only slow the rate of loss
Mechanism of changes in urine volume
Linked to adjustments in sodium (Na+) reabsorption, where water follows the movement of sodium
Role of ADH in urine volume
Allows control of water output independently of sodium by reabsorbing more water when blood osmolarity rises
Decline in blood volume and rise in osmolarity
Stimulates ADH release to produce less urine
Effect of low blood osmolarity on ADH
ADH secretion is less, kidneys reabsorb less water, and produce more urine
Fluid deficiency
Fluid imbalance occurring when output exceeds intake over a long period
Volume depletion (hypovolemia)
Loss of proportional amounts of sodium (Na+) and water; osmolarity remains normal
Causes of hypovolemia
Hemorrhage, burns, chronic vomiting or diarrhea, and Addison disease
Addison disease
Aldosterone hyposecretion
Dehydration (negative water balance)
Loss of significantly more water than sodium (Na+), leading to a rise in ECF osmolarity
Causes of dehydration
Lack of water intake, diabetes mellitus, diabetes insipidus, profuse sweating, and overuse of diuretics
Diabetes insipidus
ADH hyposecretion
Dehydration's effect on sweat
Sweat is produced by capillary filtration, leading to a drop in blood volume and pressure
Fluid shift during sweating
Blood volume is replaced by tissue fluid, which in turn pulls fluid from the ICF
Water loss breakdown for 1 L of sweat
300mL from tissue fluid and 700mL from ICF
Volume excess
Retention of both sodium (Na+) and water while ECF remains isotonic
Causes of volume excess
Aldosterone hypersecretion or renal failure
Hypotonic hydration (water intoxication)
Condition where more water than sodium (Na+) is retained/ingested, making ECF hypotonic
Cellular effect of water intoxication
Water dilutes ECF, leading to cellular swelling and dysfunction
Fluid sequestration
Excess accumulation of fluid in a particular location while TBW may be normal
Edema
The accumulation of fluid in interstitial spaces; the most common form of sequestration
Pleural effusion
Fluid accumulation in the pleural cavity, often caused by lung infections
Metabolic importance of electrolytes
They are chemically reactive and participate in metabolism
Electrical function of electrolytes
They determine electrical potential (charge difference) across cell membranes
Osmolarity of blood plasma and ICF
Both are 300mOsm/L
Resting membrane potential contribution of sodium
Sodium (Na+) is essential to the depolarizations that underlie nerve and muscle function
Sodium and cartilage hydration
Sodium (Na+) ions bound to proteoglycans of cartilage retain water
Percentage of ECF osmolarity from sodium salts
90% to 95%
Sodium-potassium pump thermogenesis
An important means of generating body heat
Role of NaHCO3 in ECF
Plays a major role in buffering pH
Adult daily sodium requirement
0.5g
Typical American sodium intake
3 to 7g/day
Primary player in sodium excretion adjustment
Aldosterone
Stimuli for aldosterone secretion
Hyponatremia, hyperkalemia, and hypotension
Effect of aldosterone on kidneys
Stimulates reabsorption of sodium and secretion of potassium
Natriuretic peptides
Hormones that inhibit sodium reabsorption, causing the kidneys to eliminate more sodium and water to lower BP
Estrogen's effect on sodium
Mimics aldosterone, causing sodium (Na+) and water retention
Progesterone's effect on sodium
Reduces sodium (Na+) reabsorption, producing a diuretic effect
Glucocorticoids' effect on sodium
Promote sodium reabsorption and causes edema
Hypernatremia
Plasma sodium concentration greater than 145mEq/L
Causes of hypernatremia
Administration of IV saline
Hyponatremia
Plasma sodium concentration less than 130mEq/L
Most abundant cation of ICF
Potassium (K+)
Potassium's role in action potentials
Involved in repolarization and hyperpolarization
Dominant determinant of cell volume
Potassium (K+)
Glomerular filtrate potassium reabsorption
90% of K+ is reabsorbed by the PCT
Potassium secretion site in kidneys
DCT and cortical portion of the collecting duct
Hyperkalemia
Plasma potassium concentration above 5.5mEq/L
Effect of fast-onset hyperkalemia
Neurons and muscle cells become more excitable; can cause cardiac arrest
Cause of fast-onset hyperkalemia
Crush injury
Effect of slow-onset hyperkalemia
Inactivates voltage-gated Na+ channels, making cells less excitable
Hypokalemia
Plasma potassium concentration less than 3.5mEq/L
Symptoms of hypokalemia
Muscle weakness, loss of muscle tone, decreased reflexes, and arrhythmias
calcium functions
Strength of skeleton, muscle contraction, second messenger, exocytosis, and blood clotting
Calsequestrin
A protein that binds calcium (Ca2+) in the smooth ER to keep it unreactive
Calcium regulation hormones
PTH, calcitriol (vitamin D), and calcitonin
Hypercalcemia
Plasma calcium greater than 5.8mEq/L
Muscular effects of extreme hypercalcemia
Muscular weakness and depressed reflexes at levels over 12mEq/L
Hypocalcemia
Plasma calcium less than 4.5mEq/L
Electrical effect of hypocalcemia
Increases membrane sodium permeability, making systems abnormally excitable
Severe hypocalcemia symptoms
Tetany, laryngospasm, and death
Distribution of magnesium (Mg2+)
54% in bone, 45% in ICF
Magnesium and ATP
Most intracellular Mg2+ is complexed with ATP
Magnesium cofactor function
Serves as a cofactor for enzymes, transporters, and nucleic acids
Normal blood levels of Mg2+
1.5 to 2.0mEq/L
Nephron segment determining magnesium retention
Ascending limb of the nephron loop
Hypermagnesemia effects
weakness, respiratory depression, and flaccid diastolic cardiac arrest