CH 26- Fluid balance

compartments of body fluids

ICF and ECF

ICF

66% of water, k, proteins, hydroten phosphate

ECF

33% of water, plasma and interstitial fluid, Na, Cl, bicarbonate

interstitial fluid

lymph, cerebrospinal fluid, humors, serous fluid, synovial fluid

example of humor

ex bile

composition of body fluids

electrolytes and non-electrolytes

electrolytes

anything that dissociate into ions in water, ±, most abundant solutes, more responsible for movement of water

examples of electrolytes

inorganic salts, acid/bases, some proteins

non-electrolytes

do not dissociate in water, no charge, make up bulk weight

non-electrolyte examples

glucose, urea, lipids

body water content factors

age, sex, body fat %

younger water content

age with higher water content

males water content

have higher water content due to muscle mass and testosterone

body fat factor with water content

lower body fat have higher water content

sources of water intake

diet and metabolic water

sources of water output

insensible and sensible water loss

examples of insensible water loss

lungs and skin

sensible water loss

sweat, urine and feces

properly hydrated ratio

water intake=output

regulating intake

hypothalamic thirst center controls thirst mechanism

activation of hypothalamic thirst center

osmoreceptors, dry mouth, decreasing BP and volume

osmoreceptors

detect changing ECF osmolality

dry mouth

salivary glands cannot draw water from blood to produce saliva

decreasing BP/volume

5-10% drop initiates mechanism

feelings of thirst stop almost immediately when you drink water

to prevent overhydration

regulating water output

obligatory water loss

examples of obligatory water loss

insensible water loss, kidneys never stop

urine output factors

fluid intake, diet, other water loss

ADH results

causes aquaporins to be inserted in collecting ducts

ADH factors

osmoreceptors and baroreceptors

osmoreceptors

monitor osmolality in ECF

baroreceptors

monitor blood pressure

deficiencies in ADH

central and nephrongenic diabetes insipidus

central diabetes insipidus

decrease in ADH by hypothalamus/posterior pituitary

effects of central/nephrogenic diabetes insipidus

polyuria, polydipsia, diluted urine, fatigue, dehydration

why fatigue

lack of water in brain

nephrogenic diabetes insipidus

ADH is released but kidneys do not respond

importance of electrolyte balance

influence water movement, excitability of neurons, membrane permeability

salt intake

mostly from diet and some from metabolic processes

salt loss

urine, feces, sweat and vomit

vomit

gastric juices are reabsorbed into bloodstream

sodium balance

NaHCO3 and NaCl account for 280 mOsm of total ECF solute

sodium is key player in ECF volume

most important for osmotic gradient, plasma membranes are impermeable

regulating Na

most is reabsorbed in PCT and nephron loop, 85%

hormonal Na regulation

aldosterone, atrial natriuretic peptide, sex hormones, glucocorticoids

aldosterone

cause reabsorption of Na in DCT and collecting ducts to increase ECF colume

atrial natriuretic peptide

decreased Na reabsorption, diuretic and natriuretic

natriuretic

process of excreting excess Na in urine

estrogen acts like

acts like aldosterone

progesterone acts as

acts as diuretic

glucocorticoids

in high plasma levels, has high aldosterone effects, edema

potassium balance importance

effects resting membrane potential, buffer

K buffer

moves in opposition of H to balance pH

principle renal cells

secrete K in DCT and collecting ducts

renal type A intercalated cells

inefficiently reabsorb K when levels are low

potassium secretion factors

plasma concentration, aldosterone

high K concentration drive K into principal cells

increased secretion and excretion K

low ECF K concentrations

promotes reabsorption

aldosterone stimulates

stimulates K secretion

adrenal cortex secretes

secretes aldosterone when K ECF are high

large shifts in Na and volume

do not affect K concentrations

renal mechanisms will

will preserve K concentration

arterial blood pH

7.35-45

alkalosis

7.45+

physiological acidosis

7.35 or lower

sources of H

diet, metabolic processes

metabolic sources of H

lactic acid, loading of CO2, phosphoric acid

regulating H

chemical buffer systems, respiratory and renal regulation

chemical buffer system

1+ compounds that resist changes in pH with strong acids/bases

basic mechanism of buffer system

release H and pH rises, bind H and pH drops

3 important buffer system

bicarbonate, phosphate, protein

bicarbonate buffer system

ECF, bicarbonate salt ties free H to carbonate acid

carbonate acid of buffer system

ties up free OH from strong base to bicarbonate acid

strong to weak acid buffer formula

HCl+ NaHCO3=H2CO3+ NaCl

strong base to weak base

NaOH+H2CO3= NaHCO3+H2O

phosphate buffer system

ICF, urine, uses weak A/B, dihydrogen phosphate, monohydrogen phosphate

protein buffer system

ICF, blood plasma, carboxyl group releases H, amine group bind H

amphoteric molecule in protein buffer system

a single protein can react as either an acid or base, envi dependent pH

rising PCO2 activates respiratory centers

RR and depth increases, pH rises with blown off CO2

decreasing Pco2 depresses respiratory centers

RR and depth decrease, pH increases with co2 accumulation

renal regulation of H

longer term acid base balance

primary mechanism for renal balance

adjusting amount of blood bicarbonate

PCT and type A intercalated cells in collecting ducts

generate new bicarbonate to reabsorb and H secretion

type B intercalated cells in collecting ducts

reabsorb H while inefficiently secreting bicarbonate from filtrate

even in alkalosis

more bicarbonate will be reabsorbed than secreted

Pco2 45+

respiratory acidosis, shallow and hypoventilation

cause of respiratory acidosis

respiratory diseases and conditions (COPD)

Pco2 less than 35

respiratory alkalosis, deep and hyperventilation

cause of respiratory alkalosis

stress, anxiety and pain

metabolic acidosis/alkalosis

does not involve CO2, bicarbonate ion imbalances

metabolic acidosis

low bicarbonate levels

metabolic acidosis causes

alcohol, long term diarrhea

metabolic alkalosis

high bicarbonate levels

metabolic alkalosis causes

excessive vomiting, excessive base intake (tumms)

blood pH

6.8-7.8

below 6.8 pH

CNS depression, permanent coma and death

7.8+ pH

overstimulated CNS, muscle tetany, restlessness, convulsions/arc, death

organ compensation

by kidney or lungs to restore blood pH

respiratory compensation

changes in RR and depth

renal compensation

kidneys compensate acid-base imbalances of lungs