Fluids, Electrolyte, And Acid-Base Homeostasis

Front 1

Describe average values for total body water in body men and women. Explain the difference in total body water.

Back 1

- Women: 50-60% H2O by weight
- Men: 60-70% H2O by weight
- men have more muscle, less adipose tissue
- adipose tissue has less H2O
- men also have denser bone

Front 2

Identify the two major fluid compartments of the body. what proportion of total body water is found in the above compartments?

Back 2

-Intracellular fluid (ECF) - 67% of body fluid, .4 x total body weight - the fluid here
- extracellular fluid - 33% of fluid; subdivisions (plasma - 20% of ECF; interstitial fluid = 80% of ECF)

Front 3

Identify the subdivisions of the extracellular fluid campartment (ECF). What proportion of teh ECF is found in each of the compartments?

Back 3

- extracellular fluid - 33% of fluid; subdivisions (plasma - 20% of ECF; interstitial fluid = 80% of ECF)

Front 4

What barrier separates the ECF and the ICF? What barrier separates the plasma and interstitial fluid?

Back 4

- cellular membrane
- the blood vessel walls

Front 5

Compare and contrast the electrolyte profile of the ECF and ICF.

Back 5

ECF - high conc (Na, Cl, HCO3-), low conc (K, HPO4, SO4)
Major cation - na+, major anion - cl-
ICF - high conc (K, HPO4, SO4, Mg, proteins) low conc (Na, Cl, HCO3)
major cation - K+, major anion - HPO4 2- and proteins

all are electrically neural, proteins and nonelectrolyte molecules also present in significan #s in all body fluids

Front 6

What is the primary difference in solute composition between the plasma and the interstitial fluid?

Back 6

- plasma proteins aren't generally in the interstitial fluid - a problem if they are

Front 7

Identify and describe the two forces responsible for fluid movement from one fluid compartment to another.

Back 7

- osmotic pressure
- hydrostatic pressure - created by BP

Front 8

What is the major force influencing movement of fluids between the ICF and the interstitial fluid?

Back 8

- osmotic pressure
- whether the other solution is isotonic, hypertonic or hypotonic

Front 9

What is the major force promoting filtration in the capillaries and lymph formation?

Back 9

- hydrostatic pressure

Front 10

What is the normal solute concentration of the plasma (expressed in mOsm/L)?

Back 10

275-299 milli-osmoles per kilogram
... according to wikipedia

Front 11

Describe a hypertonic solution and tell how it influences fluid in an adjacent compartment.

Back 11

- if you add hypertonic NaCL to the ECF, then the osmolarity of the ECF will increase, so the volume of the ECF will increase as the ICF decreases

Front 12

Describe a hypotonic solution and tell how it influences fluid in an adjacent compartment.

Back 12

- if you add a hypotonic solution of NaCl to the ECF, the osmolarity of the ECF would decrease
- initially the volune of teh ECF would increase because you added fluid to it, but then it would drop down lower than normal, as the water shifted into the ICF and into the cells

Front 13

Explain the expected changes in volune and osmolarity of the ECF and ICF in response to the following: addition of isotonic saline to the ECF, addition of hypotonic saline to the ECF, addition of hypertonic saline to the ECF.

Back 13

- isotonic - no shift; expaind the blood volume, but no swelling of tissues
hypotonic - - if you add a hypotonic solution of NaCl to the ECF, the osmolarity of the ECF would decrease
- initially the volune of teh ECF would increase because you added fluid to it, but then it would drop down lower than normal, as the water shifted into the ICF and into the cells
- hypertonic - - if you add hypertonic NaCL to the ECF, then the osmolarity of the ECF will increase, so the volume of the ECF will increase as the ICF decreases

Front 14

What is the normal daily water intake? What are the sources of this water?

Back 14

- 2.5 L/day
Sources:
- beverages, foods, metabolism

Front 15

Describe the thirst mechanism.

Back 15

- coordinated by the thirst center in hypothalamus
- Stimuli: slight inc in plasma osmolarity, dec in plasma volume or blood volume
- causes activation of thirst center = inc. perceptino of thirst - motivation to get a drink = restoration of normal plasma volume and/or osmolarity
- water moistens throat and stretches stomach

Front 16

What triggers the thirst mechanism? What slows the thirst mechanism?

Back 16

- Triggers: inc in plasma osmolarity 1-2%; dec in plasma or blood volume
- water moistening mouth and stretching stomach
- sensation of thirst can be relieved by a few sips; not triggered early enough to prevent dehydration

Front 17

Explain the avenues of water loss from the body.

Back 17

- sweat (8%)
- insensible water loss via skin and lungs (28%)
- urine (60%)

Front 18

In the body, what electrolyte is most closely tied to water balance?

Back 18

- sodium
- Na+

Front 19

ADH is the major endocrine regulator of water balance. Explain the role of ADH in maintaining water balance (i.e. role of osmoreceptors, stimuli for secretion, target cells, hormone effect, etc.)

Back 19

- osmoreceptors in hypothalamus trigger the secretion of ADH, which makes the distal tubule permeable to H2O for reabsorption
- aldosterone is also secreted and increases Na absorption in distal part of renal tubule
- ADH activates the aquaporin 2

Front 20

Describe what happens in fluid compartments (ie volume and solute) changes in dehydration. Explain the physiologic responses made to help compensate for dehydration.

Back 20

- loss happens from ECF first, then other compartments
- results in a decrease in blood volume also
- vasoconstriction from the SNS
- secrete ADH and aldosterone so that we have less urine and reabsorbe more water
- vasoconstriction on the surface, so you loose less liquid from the surface

Front 21

What is circulatory shock?

Back 21

- any condition where blood vessels are inadequately filled and blood can't circulate normally
Initial stage: dec CO, impaired tissue perfusion, hypoxia, metabolism switches to anaerobic
- non-progressive/compensatory stage - activation of cardiovascular and respiratory centers in brain stem, activation of hypothalamus leads to activ. or SNS; usu can maintain normal PO2 of tissues
- Progressive stage - tissue hypoperfusion, cardiovascular and met. impallances worsen (acidosis, dec blood pH etc), efforts of fight or flight still can't keep press high enough
- irreversible/refractory stage - cells and tissues damaged and dying

Front 22

Identify and give a general description of the four different types of circulatory shock.

Back 22

- hypobolemic - most common; from blood loss b/c of hemorrhage, vomiting, diarrhea, or burns; compensations geared towards maintining mornal MAP and tissue perfusion; blood to essential organs, dec GFR, higher CO, thirst rxn, more breathing; vasoconstriction etc
- vascular shock - blood volume normal, but vascular bed vasodilated - dec BP and poor perfusion; types (anaphylactic - allergic b/c of hystamine; neurogenic - ANS regulation failure; septic - from bacterial toxins; most common cause of death in crit. care units in USA)
- Cardiogenic shock - pumping function is so impaired that it can't circulate blood; usu. caused by MI
- Obstructive shock - when obstruction of blood flow in circulation; cause = pulmonary embolism

Front 23

Describe the physiological compensations that are made to maintain blood pressure and tissue perfusion during shock.

Back 23

- fight or flight
- activation of vasomoto centers in medula - vasoconstriction
- cardiovascular centers - higher stroke volume and HR = higher CO
- shunt blood away from non-essential organs
- kidneys = dec GFR
- RAAS system activated - inc H2O reabsorption, vasoconstriction
- osmoreceptors trigger hypothalamus secretes ADH for thirst reaction
- central and peripheral chemoreceptors activated by dec pH = inc depth and rate of breathing
- overall SNS activation

Front 24

Describe what happens in fluid compartments (ie volume and solute changes) in hypotonic hydration. Explain the physiological responses made to help compensate for hypotonic hydration.

Back 24

- water intoxication
- from ingesting lots of water quickly
- results in ECF becoming hypotonic with respect to the ICF
- result: swelling of brain tissue
- dilution of solutes in ECF
- cramping, nausia, vomiting
- lots of peeing
- treated by saline injection to pull water out of the cells so that the neurons of the brain aren't damaged

Front 25

What is an electrolyte?

Back 25

- dissociates in solution
- can ionize and conduct a current
- ex. some proteins, inorganic salts, acids, bases (inorganic and organic)
- Na, K, Ca and Mg are most significant in the body

Front 26

Explain the effects of aldosterone in teh regulation of Na and K balance.

Back 26

- K balance maintained by altering rate of tubular secretion;
- in response to high K+ levels, principle cells inc rate of K secretion, intercalated cells can alter rate of K secretion and reabsorption, but this is to preserve acid-base balance, not K balance
aldosterone affects the principle cells to increase K secretion - in DCT forces enhanced secretion coupled to H+ reabsorption,to maintain acid/base ballance.
- increases reabsorption of Na

Front 27

Name and describe the effects of the antagonistic hormones which regulate blood Ca2+ (ie. PTH and calcitonin).

Back 27

PTH - most important; triggered by low plasma Ca levels
- Effects:
-- inc. bone resorption and release of calcium and phosphate into blood
-- inc Ca absorption from GI tract
-- inc Ca reabsorption in the kidneys w/simultaneous dec. in phosphate reabsorption (gets rid of excess from bone resorption)
Calcitonin - triggered when blood Ca is high
Effects:
-- dec blood Ca - by stimulating osteoblasts and inhibiting osteoclasts
-- increased Ca storage in bone matrix

Front 28

What electrolyte concentration is measured using the pH scale?

Back 28

H+ ions

Front 29

What is teh normal range of arterial blood pH? What is the average arterial pH?

Back 29

range - 7.35-7.45
average - 7.35

Front 30

Why is it important to maintain acid-base ballance?

Back 30

- enables the body's various enzyme systems to function optimally

Front 31

- Identify the three general mechanisms involved in regulating the pH of body fluids.

Back 31

- chemical acid-base buffer system - using protein buffers, bicarbonate buffer system and phosphate buffer system
- the respiratory system - removes CO2
- renal mechanisms - alter rate of H+ secretion in urine

Front 32

Indicate the relative speeds with which each of the 3 mechanisms involved in regulating pH acts to help regulate pH

Back 32

- chemical acid-base buffer system - act almost immediately to minimize changes in pH by converting strong acids/bases to weak ones
- respiratory system - takes about 1-3 minutes to start having an effect; more powerful than all of the chemical buffers combined (1-2x their capacity)
- renal mechanisms - takes 1-3 days to effect a change in pH

Front 33

What is a buffer?

Back 33

- chemicals which function to prevent large and abrupt changes in pH of a solution
- act almost immediatly to minimize pH changes
- convert strong acids/bases to weak ones

Front 34

How do buffers help maintain acid base balance?

Back 34

- minimize pH changes by almost immediatly converting strong acids/bases to weak ones

Front 35

What characteristics of strong acids and strong bases make them more likely to cause changes in pH?

Back 35

- strong acids dissociate more in water, releasing free H+ ions

Front 36

Identify the three chemical buffering systems important in regulating the pH of body fluids. Tell where each is likely to be important.

Back 36

- Protein buffers - most abundant buffers in ICF and plasma; amino acids
- Bicarbonate buffer system - CO2 + H2O = H2CO3 = H+ + HCO3-; impt in ICF and in ECF where it's the only main one; problem, cant protect ECF from changes due to very high/low pCO2, limited by the size of the HCO3-/CO2 ratio; kidneys generate new bicarb in acidosis state
- phosphate buffer system - most important in ICF and in regulating pH of renal filtrate and urine; renal tubule is the main site of the action, stabilizing pH of urine

Front 37

What is the difference between a volatile acid and a fixed acid?

Back 37

volatile - can leave solution (CO2), can get rid of it via respiratory system
fixed acids - don't leave solution once they're produced; lactic acid, ketones, critric, phosphoric, sulfuric; can only get rid of them via renal mechanism

Front 38

How does the body normally dispose of volatile acids (CO2)? fixed acids?

Back 38

- CO2 disposed of via respiratory system
- fixed acids disposed of via renal mechanism

Front 39

Explain how the respiratory system is affected by changes in pH of arterial blood (ie. discuss the role of central chemoreceptors, medullary respiratory center, and changes in pulmonary ventilation).

Back 39

- arterial pCO2 changes, monitored by receptors
- hypercapnia indirectly activated medullary chemoreceptors via acidosis of CSF, causes hyperventilation - gets rid of CO2 and increases blood pH
- remember: CO2 + H2O = H2CO3 = H+ + HCO3-
when blood pH rises (alkalosis) respiratory centers are depressed

Front 40

Explain how changes in pulmonary ventilation (rate and depth of breathing) influence the pH of body fluids.

Back 40

- remember: CO2 + H2O = H2CO3 = H+ + HCO3-
when blood pH rises
- so by getting rid of CO2 you indirectly get rid of H+, which increases the pH when you breath faster/deeper
visa versa

Front 41

In what way can the kidneys help to compensate for changes in pH?

Back 41

- varies the rate of H+ secretion
- altering the rate of HCO3 reabsorption
- generating new HCO3-

Front 42

What are normal values for arterial pH [HCO3-] and pCO2?

Back 42

- pH - 7.35-7.45; 7.4
- HCO3- - 22-26 mEq/L; 24
- pCO2 - 35-45 mmHg; 44

Front 43

Describe the characteristics and primary causes of each of the four main types of acid-base disturbance.

Back 43

- respiratory acidosis - most common; characterized by abnormally high pCO2 and reduced pH; causes: (depression of resp brain stem by alcohol, drugs, accident; inability to exchange gas in lungs b/c of COPD, systic fibrosis; impaired ventilation)
- Respiratory alkalosis - characterized by abnormally low pCO2 and elevated pH; cause(hyperventillation b/c of abnormal response in resp centers - drugs, injury, fear, anxiety, high altitudes)
- metabolic acidosis - second most common; characterized by low arterial HCO3- and reduced pH; causes (diahrea, kidney disease, diabetes, alcohol, lactic acid, failure to excrete H+ ions
- metabolic alkalosis - fairly uncommon; characterized by high arterial HCO3- and high pH; causes (intake of alkaline substances like tums, prolonged constipation, output of acid through vomiting, gastric suctioning, diuretics)

Front 44

How does the body compensate for each of the four acid-base imballances?

Back 44

- respiratory acidosis - via renal mechanisms after exhausting buffers; inc. excretion of H+ so that intercalated cells in DT will make new bicarb; inc reabsorption of bicarb; will inc. pH, but pCO2 will still be high unless you fix the resp. problem
- respiratory alkalosis - via renal mech; slow H+ excretion and bicarb reabsorption; won't reabsorb bicarb, bicarb won't be made from glutamate, so we'll excrete less amonium; drop in pH, but pCO2 will still be low, drop in bicarb
- metabolic acidosis - resp. centers inc ventillation to dec pCO2, also renal compensation if it isn't the cause; the anion gap may be increased during compensation ( a calculated value that is normally positive, but can vary w/acid base balance; bigger than normal gap indicates a loss of bicarb w/o a concurrent increase in Cl
- metabolic alkalosis - via respiratory system; buffered in ECF and ICF; buffering maxed our, resp centers depressed to inc. CO2; kidneys reabsorb H+, remove as much HCO3- as possible, pH drops, pCO2 inc but HCO3- is still too high

Front 45

What are the steps for diagnosing acid-base imbalances? How can you tell if compensation is partial or complete?

Back 45

- compete compensation has pH in normal range
- look and see what value is out of the range
- high pCO2 = resp acid
- low pCO2 - resp alka
- low bicarb = metab acid
- high bicarb = metab alka

Front 46

hyperkalemia

Back 46

- high potassium in the body

Front 47

hypervolemia

Back 47

fluid overload
too much fluid in the body

Front 48

water intoxication

Back 48

also known as hypotonic hydration
taking in too much water...

Front 49

edema

Back 49

abnormal accumulation of fluid in interstitial space causing tissue swelling
Causes:
- inc cap hydrostatic pressure - like from a blocked vessel
- inc capillary permeability - like from inflammation
- disturbances in colloid osmotic pressure - like from hypoprotenimia (starvation, etc)

Front 50

obligatory water loss

Back 50

appx 500 mL/day
- ensures removal of toxins and other unnecessary materials from the body
- also known as facultative water loss

Front 51

facultative water loss

Back 51

appx 500 mL/day
- ensures removal of toxins and other unnecessary materials from the body
- also known as obligatory water loss

Front 52

milliequivalent (mEq)

Back 52

- the amount of a substance that will displace or combine with one mole of H+
- for Na+ 1 mEq = 1 mOsm; but for Ca2+ 1 mEq = .5 mOsm

Front 53

How is aldosterone secretion regulated?

Back 53

- triggered by low sodium or high potassium in plasma
- RAAS mechanism stimulates adrenal cortex
- aldosterone released, targets kidney tubules to reabsorb more Na + secrete more K+
- levels ballance, negative feedback

Front 54

Explain the effects of ANP in regulating blood pressure and blood volume.

Back 54

- reduces BP and blood volume by inhibiting nearly all events that promote vasoconstrictiona + Na/H2O reabsoprtion
- diuretic and natriuretic effects
- inhibits ability of collecting dubts to reabsorb Na and supresses release of ADH, renen and aldosterone
- relaxes vascular smooth muscle by inhitibint renin induced generation of angiotensin II - vasodilation

Front 55

How is ANP secretion regulated?

Back 55

- stretch of atria of heat by inc BP triggers certain cells to secrete ANP until the stretch diminishes
- negative feedback

Front 56

How does the presence of carbonic anhyrase inside the tubule cells explain the kidney's ability to help maintain pH homeostasis in body fluids?

Back 56

- carbonic anhydrase catalyzes the same rxn that it does in rbcs; H2O + CO2 = H2CO3 = H+ + HCO3-
- PCO2 in blood inc, diffuses into kidney cell
- inc. H2CO3 results, and inc H+ and HCO3- also
- the H+ diffuses into the filtrate via active transport
- HCO3- goes back into the blood, and some CO as well
- also useful to reabsorb some of the filtered bicarb for buffering (it can't diffuse across the surface, but through the rxn occuring in the filtrate, it turns into CO2, which CAN diffuse back into the cell)
- see pic p. 1012
- occurs in intercalated cells

Front 57

Explain the process through which the kidneys generate "new" bicarbonate ions. Explain the importance of this mechanism in maintaining acid/base ballance.

Back 57

Two mechanisms: excretion of buffered H+ and NH4+ excretion
- H+: CO2 combines with water in cell to form H2CO3, which is split into H and bicarb
- H is secreted into filtrate by an ATPase pump, and for each one secreted, an antiporter on the other side of cell carries the bicarb from the split into the peritubular cap. in exchange for a sodium
- secreted H combines with HPO42- in filtrate and forms H2PO4-, which is excreted in the urine
NH4: - glutamine diffuses into PCT cells, which metabolize it to NH4+ and bicarb
- NH4+, a weak acid is secreted into the filtrate, with Na coming in; it's a NH4/Na antiporter
- the bicarb from the glutamate split enters capillary via a symporter along with a Na+
- NH4 secreted in urine

Front 58

In what ways can the kidneys help to compensate for changes in pH

Back 58

- they can make new bicarb, reabsorb bicarb - this is for the buffering system
- they can excrete buffered H+, and NH4+ in the urine