WATER BALANCE

Body water content

1. Average – 50%

2. Infants – less bone and fat; 75%

3. Elderly – declines with age; 45%

4. Young men – 60%; skeletal muscle more water; 65%

5. Young women – 50%; adipose tissue least hydrated; 20%

Fluid compartments

1. ICF compartment – trillions; 2/3^rd of the water

2. ECF compartment – the rest of the water

-a. Plasma – 20% ECF

-b. Interstitial fluid – 80%; fluid between tissue cells

-c. Other fluids – lymph, CSF, synovial fluids, serous fluids, GI tract secretions

Movement between compartments

1. Osmosis – water easily moves between membranes; imbalances quickly fixed

2. Solutes – concentration determines water movement; electrolytes most important

-a. Sodium salts – most important extracellular electrolytes

-b. Potassium salts – most important intracellular electrolytes

Water gain and losses

1. Intake – 2500 ml per day

-a. Ingested fluids – 1500 ml; 60 %

-b. Foods – 750 ml; 30 %

-c. Metabolic water – 250 ml; 10 %

2. Output – 2500 ml per day

-a. Urine – 1500 ml

-b. Feces – 200 ml

-c. Expired breath – 300 ml

-d. Sweat – 100 ml

-e. Cutaneous transpiration – 400 ml; through the skin; not sweat

3. Physical activity – increased respiration and sweat; reduce urine output

4. Environment – cold air drier, increased loss through breathing; decrease sweat

5. Insensible water loss – breath and Cutaneous transpiration; not aware of it

6. Obligatory water loss – all minimum, including urine output (400 ml/day)

Regulation of water intake

1. Dehydration – increases blood osmolarity; decreases blood pressure

2. Thirst centers – in hypothalamus stimulated; osmoreceptors

3. Dry mouth – decreased salivation; ↓blood pressure; ↑osmolarity

4. Thirst – from both dry mouth and stimulation of thirst centers

5. Thirst quenched– as a result of ingesting water

-a. Short term inhibition – relieved quickly; moistened mouth distended stomach

-b. Long term inhibition – rehydration; if not thirst sensation will keep coming back

Regulation of water output

1. Osmolarity – stays the same; ↑ solute, ↑ water; ↓ solute, ↓ water
2. Sodium – chief solute; water balance closely tied to it

3. ADH – control water output independently of sodium

-a. Hypothalamic osmoreceptors - ↑ solute concentration; ↑osmolarity; ADH ↑

-b. Aquaporins – ADH causes collecting ducts to synthesize; reabsorb more water

Disorders of water balance

1. Dehydration – less water; sodium levels stay the same; ECF increased osmolarity

-a. Causes – water deprivation, diabetes insipidus (ADH hyposecretion)

-b. Symptoms - dry sticky mouth; dry flushed skin

-c. Complications – shock; neurological complication, brain cells

2. Hypovolemia – volume depletion; both water and sodium; no change osmolarity

-a. Causes – sever burns, hemorrhage, chronic vomiting and diarrhea

-b. Complication – same as for dehydration

3. Volume excess – both sodium and water in excess

-a. Causes – renal failure or aldosterone hypersecretion

-b. Complication – pulmonary and cerebral edema

4. Hypotonic hydration (water intoxication) – water in excess; sodium low

-a. Causes – renal failure; drinking large quantities of water

-b. Complications – cerebral edema; death

5. Edema - retention of fluids in interstitial space

-a. Causes - ↑ fluid out capillaries (hyper. infam.); ↓ fluid return (hypoproteinemia)

-b. Complications – tissue impairment (food O2 diffuse); circulation (low blood)

ELECTROLYTE BALANCE

Sodium

1. Function – the most pivotal ions in the body

-a. Depolarization – its influx; muscle and nerve cell function

-b. Water balance – Na ECF chief cation; where it goes water goes

-c. Sodium bicarbonate – important in acid base balance

2. Homeostasis – regulation, effects on blood pressure and osmolarity; 3 hormones

-a. Aldosterone – ↓ Na,↑ K; ↓BP (renin-angiotensin); water follows

-b. ADH – high Na in blood; ↑ water (not Na) reabsorption; Na concentration ↓

-c. ANF – hypertension stimulates release; decreases Na and water reabsorption

-d. Other hormones – estrogen mimics aldosterone; water gain, menstrual cycle

3. Hypernatremia – ECF Na >145 mEq/L

-a. Causes – dehydration in infants and confused elderly

-b. Complications – CNS, lethargy-coma; neuromuscular irritab. (twitch, convulse)

4. Hyponatremia – ECF < 130

-a. Causes – Na loss (burn, sweat); water retention

-b. Complications – brain edema; giddiness to coma; congestive heart failure

Potassium

1. Function – most cation in ICF

-a. Depolarization – with Na; nerve and muscle cells; resting potential

-b. Cofactors – protein synthesis and other metabolic processes

2. Homeostasis – closely tied to that of Na

-a. High K - ↑ secretion into filtrate in DCT and CD; K secreted as Na absorbed

-b. Aldosterone – stimulated by high K; secreted as Na reabsorbed

3. Hyperkalemia – ECF K >5.5 mEq/L

-a. Causes – renal failure; aldosterone deficits

-b. Complications – cardiac arrest; K diffuses into cells, partially depolarizes them

4. Hypokalemia – ECF K < 3.5 mEq/L

-a. Causes – vomiting, diarrhea, starvation, hyperaldoseronism

-b. Complications – cardiac arrhythmia; muscle weakness, loss of tone

Calcium

1. Function – many

-a. Skeletal system – strength and rigidity of bone; calcium phosphate salts

-b. Ionic calcium – blood clotting; exocytosis of neurotransmitters

2. Homeostasis – the functioning of two hormones

-a. PTH – released as a result of low blood Ca; increases it (3 mechanisms)

-b. Calcitonin – parafollicular cells; bone reabsorption; not as important as PTH

3. Hypecalcemia - > 5.8 mEq/ L; Na permeability reduced

-a. Causes –hyperparathyroidism; alkalosis; renal failure

-b. Complications – muscular weakness;↓reflexes; cardiac arrhythmia;↓Na perm.

4. Hypocalcemia - < 4.5 mEq/L

-a. Causes – vitamin D deficiencies; diarrhea; acidosis; pregnancy

-b. Complications – nerve, muscle irritability; tetany; larygospasm; ↑Na perm.

Magnesium

1. Functions – second most plentiful intracellular cation

-a. Coenzyme activation – for carbohydrate and protein metabolism

-b. Excitable tissue – needed for normal functioning of nerves, muscles, and heart

2. Homeostasis – poorly understood

-a. PCT reabsorption – of the Mg in the filtrate, only 3 t0 5 % is excreted

3. Hypermagnesemia - >6 mEq/L

-a. Causes – rare; excess Mg containing antacids

-b. Complications – impaired CNS; coma; respiratory depression

4. Hypomagenesemia - < 1.4 mEq/L

-a. Causes – alcoholism; loss of intestinal contents; severe malnutrition

-b. Complications – tremors; neuromuscular excitability; convulsions

Chloride

1. Function – most abundant ECF anion

-a. Osmolarity – due to its abundance

-b. Stomach acid – HCl in the stomack

-c. Chloride shift – to get bicarbonate in and out of erythrocytes

2. Homeostasis – passively follows Na as it is retained or excreted

3. Hyperchloremia – ECF > 105 mEq/L

-a. Causes – increase retention of intake

-b. Complications – metabolic acidosis; stupor and rapid breathing

4. Hypochloremia - < 95 mEq/L

-a. Causes – hyponatremia; hypokalemia

-b. Complications – metabolic alkalosis due to bicarbonate retention

Phosphates

1. Functions – relatively concentrated in ICF

-a. ATP – generation along with other nucleotide phosphates

-b. Nucleic acids – synthesis of DNA and RNA

-c. Cell membrane – phospholipids make it up

2. Homeostasis – reabsorption by PCT if levels drop too low

3. Imbalances – not much of a problem; body can tolerate wide range

Other anions

1. Bicarbonate – along with acid base balance

2. Nitrates – regulated by transport maximums in the kidneys

3. Sulfates – regulated by transport maximums in the kidneys

ACID BASE BALANCE

General comments

1. Macromolecules – enzymes, hemoglobin; denatured by too high or low pH

2. Alkalosis – arterial pH above 7.45

3. Acidosis – arterial pH below 7.35; physiological acidosis when not below 7.0

4. H⁺ sources – some ingested; most byproducts of metabolism

-a. Phosphoric acid – breakdown of phosphorus containing molecules like proteins

-b. Lactic acid – anaerobic respiration of glucose

-c. Fat metabolism – fatty acids and ketone bodies

-d. CO₂ transport – in blood as bicarbonate yields hydrogen ions

-e. Stomach HCl – must be buffered in small intestine for proper digestion

5. H+ regulation – several mechanisms; vary in length of time to mount

-a. Chemical buffer systems – act within a fraction of a second

-b. Respiratory center – within one to two minutes

-c. Renal mechanism – most potent; requires hours to more than a day

6. Acid – proton (H⁺) donor

-a. Strong acid – like HCl, H⁺ dissociates almost completely

-b. Weak acid – like carbonic acid; H⁺ and HCO₃^- not all dissociated

7. Base – proton acceptor

-a. Strong base – like NaOH; OH^- quickly tie up H⁺

-b. Weak base – like bicarbonate (HCO₃^-); doesn’t tie up all H⁺

8. Chemical buffer – releases H⁺ when pH ↑; binds H⁺ when pH ↓

Chemical buffer systems

1. Bicarbonate buffer system – mixture of sodium bicarbonate and carbonic acid

-a. NaHCO₃^- - acts as a weak base

-b. H₂CO₃ – acts as a weak acid

-c. Strong acid – HCl + NaHCO₃ → NaCl + H₂CO₃

-d. Strong base – NaOH + H₂CO₃ → NaHCO₃ +H₂O

-e. ECF – chief buffering system here

2. Phosphate buffer system – mixture of weak acid and base

-a. NaH₂PO₄ – sodium dihydrogenphosphate; weak acid

-b. Na₂HPO₄ – sodium monohydrogenphosphate; weak base

-c. Strong acid – HCl + Na₂HPO₄ → NaH₂PO₄ + NaCl

-d. Strong base – NaOH + NaH₂PO₄ → Na₂HPO₄ + H₂O

-e. ICF – more important here

-f. Renal tubules – also important here

3. Protein buffer system – side groups of the amino acids

-a. importance – about ¾ of buffering capacity; plasma and ICF

-b. Carboxyl side group (–COOH) – pH ↑; -COOH → - COO^- + H⁺

-c. Amino side group (-NH2) – pH ↓; -NH ₂ + H⁺→ -NH₃

Respiratory control of pH

1. Formula – H⁺ + HCO₃^- ↔ H₂CO₃ ↔ H₂O + CO₂ (expired)

2. High H⁺ - pulmonary ventilation increases; more CO₂ vented decreases H⁺

3. Low H⁺ - pulmonary ventilation decrease; less CO₂ vented, increase H⁺

4. Chemoreceptors – peripheral and central; stimulated by low pH and high CO₂

Renal control of pH

1. Bicarbonate binding – occurs in PCT

-a. H⁺ - secondary active transport out of PCT cell as Na transported in

-b. HCO₃^- - bicarbonate in the filtrate binds to H⁺; carbonic acid

-c. H₂CO₃ – carbonic acid

-d. Carbonic anhydrase – in brush borders of PCT cells; carbonic acid becomes

-e. H₂O – which is eliminated

-f. CO₂ – which diffuses into PCT cell

2. Conserving bicarbonate – very important; would use up stores of bicarbonate

-a. CO₂ – from blood, filtrate, and PCT cell itself combines with water

-b. Carbonic anhydrase – in PCT cell; Carbonic acid from CO₂ and H₂O; dissociate

-c. HCO₃^- - diffuses into interstitial fluid then blood of peritubular capillaries

-d. Na⁺ - pumped into interstitial fluid; into blood of peritubular capillaries

3. Alkaline reserve – bicarbonate ion must be replenished; new ones made

4. Phosphate buffer system – results in generation of new bicarbonate

-a. Collecting tubule – where this takes place; filtered bicarbonate used up

-b. Carbonic anhydrase – in collecting tubule cell generates carbonic acid

-c. Carbonic acid – dissociates into bicarbonate and Hydrogen ion

-d. HCO₃^- - newly generated; into peritubular capillaries

-e. H+ - pumped out into filtrate

-f. HPO₄^2- - monohydrogenphosphate in filtrate combines with hydrogen ion

-g. H₂PO₄^- - dihydrogen phosphate generated out in urine

5. Glutamine catabolism – deaminated, oxidated, and acidified

-a. HCO₃^- - 2 new bicarbonates for every glutamine

-b. NH₄⁺ - two new ammonium ions for every glutamine

-c. PCT – proximal convoluted tubule is where this occurs

6. Bicarbonate secretion – during alkalosis; secreted by collecting ducts

Abnormalities in acid-base balance

1. Respiratory acidosis – carbon dioxide retained; pulmonary disease

2. Respiratory alkalosis – hyperventilation; carbon dioxide lost; rarely pathological

3. Metabolic acidosis – alcoholism; diabetes (ketosis); kidney failure

4. Metabolic alkalosis – very rare; antacid overuse

5. Acidosis – pH below 7.0; CNS depression, coma, death

5. Alkalosis – pH above 7.8; overexcited; muscle tetany; convulsions; death