fluid, electrolyte, and acid-base balance (ch 25) Flashcards
body water content
babies - 75%
females - 50%
males - 60%
elderly - <50%
fluid compartments
intracellular fluid (ICF) compartment - 2/3 body H2O
extracellular fluid (ECF) compartment - 1/3 body H2O
components of ECF
20% plasma, 80% interstitial fluid
nonelectrolytes
most are organic, not ions
nonelectrolyte examples
glucose, small amounts of proteins/lipids
inorganic - urea + creatinine
electrolytes
molecules that dissociate into ions in water to conduct electrical current
electrolyte examples
salts, acids/bases, some proteins
electrolytes in ECF
major cation: Na+
major anion: Cl-
(except plasma - higher protein, lower Cl-)
electrolytes in ICF
major cation: K+
major anion: phosphate
(more soluble proteins than in plasma)
largest mass of dissolved solutes
proteins
osmolarity
solutes/volume of H2O
osmolality
solutes/mass of solvent
characteristics of fluid movement among compartments
water moves freely along osmotic gradients
body fluid osmolality almost always equal
how do changes in solute concentration affect water flow
increase in ECF osmolality –> water leaves cells
decrease in ECF osmolality –> water enters cells
types of fluid movement
between plasma and IF across capillary walls
between IF and ICF across cell membranes
how do ions move
selectively through concentration gradients
water balance
water intake must equal water output
distribution of water intake (greatest to least)
beverages>food>metabolism
distribution of water output (greatest to least)
urine>insensitive losses (skin and lungs)>sweat>feces
how is body fluid osmolality maintained
rise (decrease in body H2O): increase in ADH and thirst
fall (increase in body H2O): decrease in thirst and ADH
fluid intake is governed by the ______
hypothalamic thirst center
hypothalamic osmoreceptors detect ______
ECF osmolality
inputs to stimulate thirst
increase in plasma osmolality
dry mouth
low blood volume/BP
angiotensin II or baroreceptor input to stimulate thirst
what inhibits thirst
relief of dry mouth
activation of stomach and intestinal stretch receptors
how does ADH influence water output
an increase in body osmolality stimulates ADH, decreasing urine output
disorders of water balance
dehydration
water intoxication
edema
dehydration causes
increased sweat
decrease fluid to drink
vomiting
diarrhea
diuretic medication
alcohol
burns
signs and symptoms of dehydration
thirst
dry mouth
decreased urine output
dry skin
results of dehydration
weight loss –> decreased BP –> confusion –> hypovolemic shock
causes of water intoxication
renal insufficiency
rapid excess water ingestion
results of water intoxication
decrease in ECF osmolality –> hyponatremia –> osmosis of H2O into body cells –> swelling of cells –> cerebral swelling –> headache –> death
treatment of water intoxication
hypertonic saline solution via IV
what is edema
too much interstitial fluid, leading to tissue (not cell) swelling from fluid coming out of the blood into the ICF
causes of edema
increased capillary hydrostatic pressure or permeability
low blood proteins
blocked (or surgically removed) lymphatic vessels
central role of sodium
controls ECF volume and water distribution - therefore determines BP
which movement mechanisms are coupled to the sodium ion
gradients, glucose, amino acids
how is sodium balance regulated
no known receptors, so Na+ levels in blood fluids is linked to blood pressure and volume
how is sodium mainly reabsorbed
by the kidney/PCT
aldosterone causes
reabsorption of Na+ in the DCT and collecting ducts
increased K+ secretion into urine
main trigger for aldosterone release
angiotensin II via the renin angiotensin system
alternative trigger for aldosterone release
elevated levels of K+
how long for aldosterone to take effect
slowly - hours to days
atrial natriuretic peptide is released by
atrial cells in response to stretch in the atria (which increases BP and venous return)
function of ANP
decreases hormones (ADH, renin/angiotensin II, aldosterone)
increases excretion of Na+ and H2O in urine, decreasing BP
estrogens act like
aldosterone
progesterone blocks
aldosterone
function of glucocorticoids
increase Na+ reabsorption
when can glucocorticoids promote edema
when given at pharmaceutical levels to decrease inflammation
importance of potassium
affects RMP in neurons and muscle cells (specifically heart muscle)
hyperkalemia
increase in K+ ECF, leading to decreased RMP (depolarization of cell)
hypokalemia
decrease in K+ ECF, leading to increased RMP (hyperpolarization of cell)
hyperkalemia and hypokalemia lead to
disrupted electrical conduction in the heart - can result in arrythmias, arrest, or death
regulation of potassium balance
controlled in collecting ducts by regulating the amount of secretion into filtrate
most important factor is concentration in ECF
adrenal cortical cells are directly sensitive to
the K+ content of ECF to cause aldosterone release
main storage of calcium in the body (99%)
in bones as calcium phosphate salts
calcium in the ECF is important for
blood clotting
cell membrane signals
secretion of NTs
neuromuscular excitability
hypocalcemia leads to
increased excitability
hypercalcemia leads to
inhibition - can lead to arrythmias in the heart
calcium balance is controlled by
parathyroid hormone from the parathyroid gland
PTH and bones
results in overall breakdown, leading to calcium being released into the blood
PTH and kidneys
increases calcium reabsorption from filtrate (causes retention)
PTH and the small intestine
activates vitamin D, leading to Ca++ reabsorption from food
Cl- is a major anion in _____
ECF
function of chloride
helps maintain the osmotic pressure of blood and ECF
under normal pH conditions, 99% of Cl- is with
Na+
normal pH of body fluids
7.35-7.45
alkalosis or alkalemia
arterial pH >7.45
acidosis or acidemia
arterial pH < 7.35
most H+ is produced by
metabolism
phosphoric acid comes from
phosphate in H2O into ECF
lactic acid comes from
anaerobic respiration of glucose
fatty acids and ketones come from
fat metabolism
carbonic acid is made when
CO2 combines with water
acid-base balance is regulated by
chemical buffer systems (milliseconds)
respiratory centers in the brain (minutes)
renal mechanisms (hours to days)
strong acids + water
complete dissociation (H+Cl- -> H+ + Cl-)
weak acids + water
partial dissociation (H2CO3 <-> H+ + HCO3-)
strong bases + water
easily dissociate (Na+OH- -> Na+ + OH-)
weak bases + water
accept H+ slowly (Na+HCO3-)
chemical buffer systems are combinations of
weak acid and weak base
most important buffer system
bicarbonate buffer system
bicarbonate buffer system
mixture of carbonic acid (weak) and salts of bicarbonate (weak bases)
strong acid + bicarbonate buffer system
strong acid + weak base -> weak base + salt (NA+OH- + H2CO3 ->Na+HCO3- + H2O)
strong base + bicarbonate buffer system
strong base + weak acid -> weak base + water (HCl + NaHCO3 -> H2CO3 + NaCl)
phosphate buffer system
most important in urine
sodium salts of dihydrogen phosphate is a weak acid
sodium salts of monohydrogen phosphate is weak base
protein buffer system
most important inside cells and in plasma
proteins can function as both a weak acid or base
pH and the protein buffer system
rise: carboxyl (COOH) groups weaken base when more base is added to weak acid
fall: NH2 groups weaken acid when more acid is added to weak base
respiratory mechanism of adjusting pH
adjusting CO2
acidic - increase respiration
basic - decrease respiration
renal mechanism of adjusting pH
peeing out acid or base
reabsorbing/generating new HCO3- = H+ excretion
excreting HCO3- = H+ retention
excreting ammonium ion (excess acid)
the ammonium ion is created from
amino acid glutamate
causes of respiratory acidosis
hypoventilation
pulmonary disease
restriction
drug overdose
alcohol poisoning
causes of respiratory alkalosis
hyperventilation
panic attacks
high altitudes
indicator of respiratory acidosis or alkalosis
blood CO2
indicator of metabolic acidosis or alkalosis
abnormal HCO3- levels
metabolic acidosis
low pH and bicarbonate
causes of metabolic acidosis
ketosis
diarrhea (loss of base)
alcohol (acetic acid + ketones)
metabolic alkalosis
high pH and bicarbonate
causes of metabolic alkalosis
vomiting (loss of acid)
antacid overdose
