KAAP310 EXAM 2 - Fluid, Electrolyte, and Acid-Base Balance

percentage of body fluids in each fluid compartment

65% ICF and 35% ECF

- ECF is divided into...

25% tissue (interstitial) fluid

8% blood plasma and lymph

2% transcellular fluid - CSF, synovial, peritoneal, pleural, etc.

how water moves from one fluid compartment to another

Osmosis from one fluid compartment to another is determined by relative concentration of solutes in each compartment

Most abundant solute particles are the electrolytes - sodium in ECF and potassium in ICF

sensible water loss

noticeable output, thorugh urine and sufficient sweating to produce wetness of the skin

insensible water loss

output through breath and cutaneous transpiration, we are not aware of it

obligatory water loss

unavoidable output, expired air, cutaneous transpiration, fecal moisture, minimum urine output

daily water gain

Metabolic water - 200 mL/day, produced as a byproduct of dehydration synthesis reactions and aerobic respiration

Preformed water - ingested in food (700 mL/day) and drink (1,600 mL/day)

daily water loss

1,500 mL/day is excreted as urine

200 mL/day excreted in feces

300 mL/day is lost in expired breath

100 mL/day of sweat is secreted by a resting adult at ambient air temperature

400 mL/day is lost as cutaneous transportation - water that diffuses through epidermis and evaporates

hypothalamus and thirst

has osmoreceptors that respond to angiotensin II and rising osmolarity of ECF (signs of dehydration)

communicate with other neurons that produce ADH, and cerebral cortex to produce conscious sense of thirst

sympathetic output from hypothalamus inhibits salivary glands to produce sense of thirst

short term mechanisms by which thirst is satiated

moistening of mouth and throat, protective and anticipatory

distension of stomach - helps reduce thirst senesation

long term mechanisms by which thirst is satiated

plasma becomes less concentrated and osmoreceptors turn off thirst signal

water increases blood volume, which triggers baroreceptors to reduce renin and ADH secretion, shutting off thirst

electrolytes function

chemically reactive and participate in metabolism, determine electrical potential across cell membranes, and strongly affect the body's water content and distribution

Major cations: sodium, potassium, calcium, magnesium, and hydrogen

Major anions: chloride, bicarbonate, and phosphates

ECF concentration of electrolytes

Sodium: 145 mEq/L

Potassium: 4

Calcium: 5

Magnesium: 2

Chloride: 103

Potassium: 4

ICF concentrations of electrolytes

Sodium: 12

Potassium: 150

Calcium: <1

Magnesium: 40

Chloride: 4

Potassium: 75

physiological functions of sodium

Fluid balance, nerve impulse conduction, muscle contraction, acid-base balance, nutrient transport (drives secondary active transport of glucose/amino acids in the gut and kidneys)

how sodium is regulated by aldosterone

increases Na reabsorption in DCT and CD, increases blood volume and pressure

how sodium is regulated by ADH

promotes water reabsorption, dilutes Na concentration by retaining water

High concentration stimulates ADH release, the kidneys reabsorb more water, which slows down any further increase in blood sodium concentration

how sodium is regulated by natriuretic peptides

inhibit sodium and water reabsorption and secretion of renin/ADH

kidneys eliminate more water and sodium and lowers blood pressure

Hypernatremia

Causes: water loss, inadequate water intake, excess Na+ intake (rare)

Effects: cellular dehydration, confusion, irritability, seizures, coma, thirst, dry mucous membranes, hypotension

hyponatremia

Causes: excess water intake or retention, diuretics, vomiting/diarrhea, heart failure, kidney or liver disease

Effects: cellular swelling, brain swelling (headache, confusion, seizures, coma), muscle cramps, nausea

physiological functions of potassium

Resting membrane potential, nerve impulse transmission, skeletal and cardiac muscle contraction, acid-base balance, cellular function (osmotic balance, enzyme activity, cellular metabolism)

how potassium is regulated by the kidneys

about 90% of K is secreted in the urine

K is filtered in glomerulus, reabsorbed in proximal tubule, and secreted in DCT and CDs

how potassium is regulated by aldosterone

increases Na reabsorption and K secretion in DCT and CDs

activates Na/K ATPase and K channels

promotes urinary K loss

hyperkalemia

Causes: renal failure, aldosterone deficiency, acidosis, cell lysis, ACE inhibitors, K+-sparing diuretics

Effects: depolarizes resting membrane potential, cardiac arrhythmias, muscle weakness, paralysis, numbness or tingling

hypokalemia

Causes: Diuretics (especially loop and thiazide), vomiting/diarrhea, hyperaldosteronism, alkalosis, inadequate intake

Effects: hyperpolarizes cells, muscle cramps/weakness, fatigue, cardiac arrhythmias (U waves, flattening T waves), constipation

physiological functions of calcium

Muscle contraction, nerve transmission, blood clotting, bone structure, enzyme activity/signaling, membrane stability

why cells maintain low calcium level

High calcium levels in cytoplasm is a powerful signaling trigger, so it is low to prevent erratic or excessive activation of cellular processes

Prolonged high calcium levels can cause mitochondrial dysfunction, enzyme overactivation, and even apoptosis

Require high concentration of phosphate ions, and if calcium and phosphate were both concentrated, calcium phosphate crystals would precipitate

how calcium is regulated by PTH

Increases bone resorption -> releases calcium and phosphate

Increases renal calcium reabsorption, decreases phosphate reabsorption

Stimulates calcitriol production -> enhances intestinal calcium absorption

how calcium is regulated by calcitriol

Increases intestinal calcium and phosphate absorption

Synergizes with PTH to increase bone resorption and renal calcium retention

how calcium is regulated by calcitonin

Decreases bone resorption by inhibiting osteoclasts

Renal calcium excretion increase

Protective against hypercalcemia

hypercalcemia

Causes: hyperparathyroidism, malignancy, excess vitamin D, thiazide diuretics

Effects: kidney stones, bone pain, abdominal pain, constipation, polyuria, dehydration, confusion, lethargy

hypocalcemia

Causes: hypoparathyroidism, vitamin D deficiency, renal failure, magnesium deficiency

Effects: tetany, cramps, paraesthesias, seizures, prolonged QT interval

normal pH of blood

Normal pH = 7.35-7.45

Crucial because acids are a constant challenge to enzyme function, homeostasis, and survival

bicarbonate buffer system

CO2 + H2O -> H2CO3 -> H+ + HCO3-

If there is too much acid, the buffer system moves to the left to breathe out CO2

If there is too much base (OH-), the kidneys excrete HCO3- and move the reaction to the right which elevates H+ concentration

Fast, works in blood plasma and ECF

Regulated by lungs and kidneys

phosphate buffer system

H2PO4- -> H+ + HPO4-

Proceed to right to liberate H+ and lower pH, or proceed to left to bind H+ and raise pH

Stronger buffering effect than equal amount of bicarbonate buffer

protein buffer system

accounts for 3/4ths of all chemical buffering in the body fluids

Buffering abilities of proteins is due to certain side groups

-Carboxyl side groups release H+ and lowers pH

-Amino side groups bind H+ and raises pH

how respiratory system buffers pH

Adjusts pH by raising or lowering the rate and depth of breathing

Bicarbonate buffer system ^

how renal tubule secretes acid

H+ is secreted into tubular fluid via Na+/H+ antiporters and H+-ATPase pumps on apical side

Inside tubule cells, CO2 + H2O -> H2CO3 -> H+ + HCO3- via carbonic anhydrase

H+ is secreted into the tubule, HCO3- is reabsorbed into the blood

why is urine bicarbonate free?

Kidneys reabsorb nearly all filtered bicarbonate (HCO3-) in proximal tubule to maintain systemic pH

Healthy urine contains little bicarbonate - the body conserves it to buffer the blood

why acid secretion is linked to sodium reabsorption

Na+/H+ antiporter in proximal tubule reabsorbs Na+ from filtrate in exchange for secreting H+

Helps with sodium homeostasis and acid-base balance

role of disodium hydrogen phosphate in buffering urinary acid

Once H+ is secreted into the urine, it must be buffered to prevent the urine from becoming dangerously acidic

NA2HPO4 acts as a base, accepting H+ to form NaH2PO4

Traps H+ in non-diffusible form, allowing it to be safely excreted in the urine

role of ammonia in buffering urinary acid

Produced by renal tubular cells from glutamine metabolism

Diffuses into the tubule and binds H+ to form ammonium