1 ADVANCED PHYSIOLOGY FLUID & ELECTROLYTES PART 2 Instructor Terry Wiseth

1

ADVANCED ADVANCED PHYSIOLOGYPHYSIOLOGY

FLUID & ELECTROLYTESFLUID & ELECTROLYTES

PART 2PART 2

Instructor Terry WisethInstructor Terry Wiseth

2

ELECTROLYTE BALANCEELECTROLYTE BALANCEThe exchange of interstitial and

intracellular fluid is controlled mainly by the presence of the electrolytes sodium and potassium

NaNa++KK++

NaNa++KK++

NaNa++ KK++

NaNa++

KK++

3

ELECTROLYTE BALANCEELECTROLYTE BALANCEPotassium is the chief intracellular

cation and sodium the chief extracellular cation

Because the osmotic pressure of the interstitial space and the ICF are generally equal, water typically does not enter or leave the cell

KK++

NaNa++

4

ELECTROLYTE BALANCEELECTROLYTE BALANCEA change in the concentration of either

electrolyte will cause water to move into or out of the cell via osmosis

A drop in potassium will cause fluid to leave the cell whilst a drop in sodium will cause fluid to enter the cell

KK++

H2O

H2O

H2O H2O

H2O

H2O

H2O H2O

KK++

KK++

KK++

NaNa++

NaNa++

NaNa++

NaNa++

Click to seeanimation

5

ELECTROLYTE BALANCEELECTROLYTE BALANCEA change in the concentration of either

electrolyte will cause water to move into or out of the cell via osmosis

A drop in potassium will cause fluid to leave the cell whilst a drop in sodium will cause fluid to enter the cell

KK++

H2OH2O

H2O H2O

H2O

H2O

H2O H2O

KK++

KK++

KK++

NaNa++

NaNa++NaNa++

NaNa++


6

ELECTROLYTE BALANCEELECTROLYTE BALANCEAldosterone, ANP and ADH regulate

sodium levels within the body, whilst aldosterone can be said to regulate potassium

KK++

NaNa++

aldosterone

ADH

ANP

7

ELECTROLYTE BALANCEELECTROLYTE BALANCE

Sodium (NaNa++) ions are the important cations in extracellular fluid

Anions which accompany sodium are chloride (ClCl--) and bicarbonate (HCOHCO33

--)

Considered an indicator of total solute concentration of plasma osmolality

NaNa++

HCOHCO33--ClCl--

8

H2OH2O

H2OH2OH2O

H2O

ELECTROLYTE BALANCEELECTROLYTE BALANCESodiumSodium ions are osmotically

important in determining water movements

A discussion of sodium must also includeChlorineChlorineBicarbonateBicarbonateHydrogen ionsHydrogen ions

PotassiumPotassium and calciumcalcium serum concentrations are also important electrolytes in the living system

H2O

H2O

H2O

H2O

H2O

H2OH2OH2OH2O

9

ClickHypercalcemiaHypercalcemia - elevated calcium levels

HypokalcemiaHypokalcemia -- lowered calcium levels

ClickHyperkalemiaHyperkalemia -- elevated potassium levels

HypokalemiaHypokalemia ---- lowered potassium levels

HypernatremiaHypernatremia - elevated sodium levels

HyponatremiaHyponatremia -- lowered sodium levels

ELECTROLYTE BALANCESELECTROLYTE BALANCES

10

HYPERNATREMIAHYPERNATREMIANormal range for blood levels of

sodium is app. 137 - 143 meq/liter

HypernatremiaHypernatremia refers to an elevated serum sodium level (145 -150 meq/liter)

Increased levels of sodium ions are the result of diffusion and osmosis

Na+

SODIUM PRINCIPLESSODIUM PRINCIPLES1) Sodium ions do not cross cell

membranes as quickly as water does

Na+

H2O

H2O H2O

H2O

H2O

Na+

12

SODIUM PRINCIPLESSODIUM PRINCIPLES2) Cells pump sodium ions out of

the cell by using sodium-potassium pumps

Na+

Na+

Na+

Na+

13

SODIUM PRINCIPLESSODIUM PRINCIPLES3) Increases in extracellular sodium

ion levels do not change intracellular sodium ion concentration

Na+Na+

Na+Na+

Na+

Na+

Na+

Na+

Na+

Na+

Na+

Na+

Na+

Na+

Na+

Na+

Na+

Na+

Na+

Na+

14

RESULTS OF RESULTS OF HYPERNATREMIAHYPERNATREMIA

1) Water is osmotically drawn out of the cells

Resulting in dehydration

2) Increase in extracellular fluid volumeExtracellular

fluid volume

Intracellular fluid

volume

15

CNS REACTION TO CNS REACTION TO HYPERNATREMIAHYPERNATREMIA

In the CNS tight junctions exist between endothelial cells of the capillary walls

These junctions restrict diffusion from capillaries to the interstitium of the brainblood-brain barrierblood-brain barrier

Increased levels of sodium ions in the blood does not result in increased sodium ions in brain interstitial fluid

16

CNS REACTION TO CNS REACTION TO HYPERNATREMIAHYPERNATREMIA

As the result of an osmotic gradient, water shifts from the interstitium and cells of the brain and enters the capillariesThe brain tends to shrink and

the capillaries dilate and possibly rupture

Result is cerebral hemorrhage, blood clots, and neurological dysfunction

H2

O

17

CNS PROTECTIVE CNS PROTECTIVE MECHANISMMECHANISM

There is an unknown mechanism that protects the brain from shrinkage

Within about 1 day

Intracellular osmolality of brain cells increases in response to extracellular hyperosmolality

18

CNS PROTECTIVE CNS PROTECTIVE MECHANISMMECHANISM

Idiogenic osmoles accumulate inside brain cellsK+, Mg+ from cellular binding sites

and amino acids from protein catabolism

These idiogenic osmoles create an osmotic force that draws water back into the brain and protects cells from dehydration

H2

O

19

CAUSES OF CAUSES OF HYPERNATREMIAHYPERNATREMIA1) Water loss

2) Sodium ion overloadMost cases are due to

water deficit due to loss or inadequate intake

Infants without access to water or increased insensible water loss can be very susceptible to hypernatremia

20

WATER LOSSWATER LOSSDiabetes insipidus caused by

inadequate ADH or renal insensitivity to ADH results in large urinary fluid lossIncreased fluid loss also occurs as the

result of osmotic diuresis (high solute loads are delivered to the kidney for elimination)

21

Glucose

Glucose

Glucose

WATER LOSSWATER LOSSdiabetes mellitus results in loss of

fluids as well by creating an osmotic pull (increased urine solute concentration) on water into the tubules of the kidney

Glucose

Glucose

Glucose

Glucose

Glucose

Glucose

Glucose

GlucoseH2O

H2OH2O

H2O

H2O

H2O

H2O H2O

H2O

H2O

H2OH2O

22

Glucose

Glucose

Glucose



Glucose

Glucose

Glucose

Glucose

Glucose

Glucose

Glucose

GlucoseH2O

H2OH2O

H2O

H2O

H2O

H2O H2O

H2O

H2O

H2OH2O

23

Glucose

Glucose

Glucose



Glucose

Glucose

Glucose

Glucose

Glucose

Glucose

Glucose

GlucoseH2O

H2OH2O

H2O

H2O

H2O

H2O H2O

H2O

H2O

H2OH2O

24

Glucose

Glucose

Glucose



Glucose

Glucose

Glucose

Glucose

Glucose

Glucose

Glucose

GlucoseH2O

H2OH2O

H2O

H2O

H2O

H2OH2O

H2O

H2O

H2OH2O

25

Glucose

Glucose

Glucose



Glucose

Glucose

Glucose

Glucose

Glucose

Glucose

Glucose

GlucoseH2O

H2OH2O

H2OH2O

H2O

H2OH2O

H2O

H2O

H2OH2O

26

Glucose

Glucose

Glucose



Glucose

Glucose

Glucose

Glucose

Glucose

Glucose

Glucose

GlucoseH2O

H2OH2O

H2OH2O

H2O

H2OH2O

H2O

H2O

H2OH2O

27

Glucose

Glucose

Glucose



Glucose

Glucose

Glucose

Glucose

Glucose

Glucose

Glucose

GlucoseH2O

H2OH2O

H2OH2O

H2O

H2OH2O

H2O

H2O

H2OH2O

28

Glucose

Glucose

Glucose



Glucose

Glucose

Glucose

Glucose

Glucose

Glucose

Glucose

GlucoseH2O

H2OH2O

H2OH2O

H2O

H2OH2O

H2O

H2O

H2OH2O

Re-animate

29

WATER LOSSWATER LOSSHigh protein feedings by a stomach

tube create high levels of urea in the glomerular filtrate producing an osmotic gradient the same as glucose does and increased urinary output results

30

SODIUM EXCESSSODIUM EXCESS

Occurs less frequently than water loss

Retention or intake of excess sodiumex: IV infusion of hypertonic sodium ion

solutions

Aldosterone promotes sodium and water retention by the kidneyHigh levels of aldosterone may result in

mild hypernatremia

31

CAUSES OF HYPERNATREMIACAUSES OF HYPERNATREMIACAUSE COMMENTS

essential hypernatremia disorder in which thirst is impaired

fever increased insensible fluid loss

coma inadequate fluid intake

hot environment, or strenuousexercise

sweat, hypotonic fluid loss

vomiting often a hypotonic fluid loss

diarrhea often a hypotonic fluid loss

pituitary diabetes insipidus deficiency of ADH; excessive fluidloss

nephrogenic diabetes mellitus renal tubules insensitive to ADH;excessive urinary loss

uncontrolled diabetes mellitus glucose in glomerular filtrate;osmotic diuresis

large amounts of protein and aminoacids given by nasogastric tube

urea is a product of proteinmetabolism; urea causes osmoticdiuresis

excessive intravenous infusion ofhypertonic sodium salt solutions

administration of excessive sodiumions

mannitol used as diuretic mannitol in glomerular filtrate;osmotic diuresis

32

TREATMENT OF TREATMENT OF HYPERNATREMIAHYPERNATREMIA

Re-hydration is the primary objective in most cases

Decreases sodium concentrations

A point of concern is whenand how rapid there-hydration occurs

33


After 24 hours the brain has responded by producing idiogenic osmoles to re-hydrate brain cells

If this adaptation has occurred and treatment involves a rapid infusion of dextrose for example:

There is danger of cerebraledema with fluid beingdrawn into brain tissues

34


Treatment is best handled by giving slow infusions of glucose solutions

This dilutes high plasmasodium ion concentrations

35


Ideally the goal is to avoid overloading with fluid and to remove excess sodium

Diuretics can be used to induce sodium and water diuresisHowever if kidney function is not normal

peritoneal dialysis may be required

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Defined as a serum sodium ion level that is lower than normal

Implies an increased ratio ofwater to sodium in extracellularfluid

Extracellular fluid is more dilute than intracellular fluid

Results in a shift of water into cells

HYPONATREMIAHYPONATREMIA

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CNS RESPONSE TO CNS RESPONSE TO HYPONATREMIAHYPONATREMIA

Brain cells lose osmoles creating a higher extracellular solute concentration

Effect is to protect against cerebral edema by drawing water out of the brain tissue

38

GENERAL RESPONSE TO GENERAL RESPONSE TO HYPONATREMIAHYPONATREMIA

Suppression of thirst

Suppression of ADH secretion

Both favor decreasing wateringestion and increasingurinary output

39

SYMPTOMS OF SYMPTOMS OF HYPONATREMIAHYPONATREMIA

Primarily neurological (net flux of water into the brain)

Sodium ion levels of 125 meq / liter125 meq / liter are enough to begin the onset of symptoms

Sodium ion levels of less than 110110 meq / litermeq / liter bring on seizures and coma

40

HYPONATREMIAHYPONATREMIA

Produced by:

1) A loss of sodium ions 1) A loss of sodium ions 2) Water excess2) Water excess

Water excess can be due to:Ingestion Renal retention

41

DILUTIONAL EFFECTDILUTIONAL EFFECT

1) Isotonic fluid loss1) Isotonic fluid loss2) Antidiuretic hormone 2) Antidiuretic hormone

secretionsecretion3) Acute or chronic renal failure3) Acute or chronic renal failure4) Potassium ion loss4) Potassium ion loss5) Diuretic therapy5) Diuretic therapy

H2O

H2O

H2OH2O

H2O

H2O

Na+

Na+Na+

H2O

H2O

H2O

H2O

H2O

H2O

H2O

H2ONa+

Na+

Na+

Na+

Na+

H2O

H2O

H2O

H2O

H2O

42

DILUTIONAL EFFECTDILUTIONAL EFFECT

1) 1) Isotonic fluid lossIsotonic fluid lossBurns, fever, hemorrhageIndirect cause of hyponatremiaAny volume loss stimulates thirst and

leads to increased water ingestionThus isotonic fluid loss can cause

hyponatremia not because of sodium loss but because of increased water intake

43

DILUTIONAL EFFECTDILUTIONAL EFFECT2) 2) Antidiuretic hormone secretionAntidiuretic hormone secretion

Enhances water retention

3) 3) Acute or chronic renal failureAcute or chronic renal failureThe kidney fails to excrete waterCan lead to hyponatremia

44

DILUTIONAL EFFECTDILUTIONAL EFFECT4) 4) Potassium ion lossPotassium ion loss

Potassium ions are the predominant intracellular cations

When they are lost they are replaced by diffusion of intracellular potassium into extracellular fluid

Electrical balance is maintained by the diffusion of sodium ions into the cells in exchange for potassium ions

Thus a loss of extracellular sodium is realized and hyponatremia may ensue

45

POTASSIUM ION POTASSIUM ION LOSSLOSS

KK++

NaNa++

NaNa++

KK++

KK++

KK++

1) extracellular1) extracellular potassium losspotassium loss

2) diffusion of potassium 2) diffusion of potassium ions into extracellular ions into extracellular

compartmentscompartments

3) intracellular electrical balance 3) intracellular electrical balance is maintained by diffusion of is maintained by diffusion of

sodium ions into cellssodium ions into cells

plasmaplasmainterstitial fluidinterstitial fluid

cellcell

46

POTASSIUM ION POTASSIUM ION LOSSLOSS

KK++

NaNa++

KK++KK

++ KK++

PlasmaPlasmaInterstitial fluidInterstitial fluid

CellCell

KK++

KK++

NaNa++

NaNa++


47

DILUTIONAL EFFECTDILUTIONAL EFFECT5) 5) Diuretic therapyDiuretic therapy

Common cause of hyponatremia

Loss of sodium and potassium often occurs in addition to fluid loss

48

CAUSES OF CAUSES OF HYPONATREMIAHYPONATREMIACAUSE COMMENTS

psychogenic polydipsia excessive ingestion of water

syndrome of inappropriate secretion of ADH

ADH causes renal water retention

Addison’s disease aldosterone deficiency

K+ losses from extracellular fluid

K+ move out of cells to replace losses; Na+ move into cells to maintain electrical neutrality

49

REACTIONS TO REACTIONS TO HYPONATREMIAHYPONATREMIA

Increased Na+

Osmoreceptorsinhibited

Decreased ADHrelease

Decreased Thirst

Increased urinary H2O loss

Decreased H2O gain

Decreased Na+

HomeostasisNormal Na+

Osmoreceptorsstimulated

Increased ADHrelease

Increased Thirst

Additional H2Odilutes Na+

H2O lossconcentrates Na+

Decreased urinary H2O loss

Increased H2O gainClick to viewincreased Na+

Click to viewdecreased Na+

50

HYPERKALEMIAHYPERKALEMIANormal serumserum potassium level (3-5

meq / liter)As compared to NaNa++ (142 meq / liter)

IntracellularIntracellular levels of potassium (140-150 meq / liter)This high intracellular level is

maintained by active transport by the sodium-potassium pump

K+

51

NaNa++ / K / K++ Pump PumpCells pump K+ ions in and Na+ ions

out of the cell by using sodium-potassium pumps

Na+

Na+

Na+

Na+

K+

K+

K+

K+

52

HYPERKALEMIAHYPERKALEMIAHyperkalemiaHyperkalemia is an elevated serum

potassium (KK++) ion levelA consequence of hyperkalemia is

acidosisacidosis an increase in HH++ ions in body fluids

Changes in either KK++ or HH++ ion levels causes a compartmental shift of the other

K+

53

HYPERKALEMIAHYPERKALEMIAWhen hyperkalemia develops

potassium ions diffuse into the cellThis causes a movement of HH++ ions out

of the cell to maintain a neutral electrical balance

As a result the physiological response to hyperkalemia causes acidosis

K+

K+

K+

K+

K+

K+H+

H+

H+

H+

H+H+

H+H+

H+

HYPERKALEMIA

54

HYPERKALEMIAHYPERKALEMIAThe reverse occurs as wellThe body is protected from harmful

effects of an increase in extracellular HH++ ions (acidosis) HH++ ions inside the cells are tied up by

proteins (PrPr --)This causes a shift of potassium

ions out of the cells

55

HYPERKALEMIAHYPERKALEMIAThe reverse occurs as wellThe body is protected from harmful

effects of an increase in extracellular HH++ ions (acidosis) HH++ ions inside the cells are tied up by

proteins (PrPr --)This causes a shift of potassium

ions out of the cells

H+

H+

H+

H+

H+

H+H+

H+

H+

K+

K+K+

K+K+

K+

ACIDOSIS

56

HYPERKALEMIAHYPERKALEMIASummarized:

Hyperkalemia causes acidosis Acidosis causes hyperkalemia

HYPERKALEMIAH+

H+

H+

H+

H+

H+

H+ H+

K+

K+

K+

K+

K+

K+

K+ K+

ACIDOSIS

57

HYPERKALEMIAHYPERKALEMIASummarized:

Hyperkalemia causes acidosis Acidosis causes hyperkalemia

HYPERKALEMIAH+

H+

H+

H+

H+

H+

H+ H+

K+

K+

K+

K+

K+

K+

K+ K+

ACIDOSIS

58

SYMPTOMS OF SYMPTOMS OF HYPERKALEMIAHYPERKALEMIA

Muscle contraction is affected by changes in potassium levels

Hyperkalemia blocks the transmission of nerve impulses along muscle fibersCauses muscle weakness and

paralysisCan cause arrhythmia's and

heart conduction disturbances

59

CAUSES FOR CAUSES FOR HYPERKALEMIAHYPERKALEMIA

1) Increased input of potassium

2) Impaired excretion of potassium

3) Impaired uptake of potassium by cells

60

INCREASED INPUTINCREASED INPUTA) Intravenous KClKCl infusion

B) Use of KK++ containing salt substitutes

C) Hemolysis of RBC during blood transfusions with release of KK++

D) Damaged and dying cells release KK++

Burns, crush injuries, ischemia

E) Increased fragility of RBC

61

CELLULAR-EXTRACELLULAR CELLULAR-EXTRACELLULAR SHIFTSSHIFTS

Insulin deficiency predisposes an individual to hyperkalemia

Cellular uptake of KK++ ions is enhanced by insulin, insulin, aldosterone and epinephrinealdosterone and epinephrineProvides protection from

extracellular KK++ overload

Insulin K+

K+

K+

K+

K+ K+

Click to viewanimation

62

CELLULAR-EXTRACELLULAR CELLULAR-EXTRACELLULAR SHIFTSSHIFTS

Insulin deficiency represents decreased protection if the body is challenged by an excess of K+ ions

In the absence of aldosterone there is loss of Na+ in the urine and renal retention of K+

63

HYPERKALEMIC PERIODIC HYPERKALEMIC PERIODIC PARALYSISPARALYSIS

Inherited disorder in which serum KK++ level rise periodicallyCaused by a shift of KK++ from

muscle to blood in response to ingestion of potassium or exercise

Reasons for the shift arenot clear

Attacks are characterizedby muscle weakness

64

RENAL INSUFFICIENCYRENAL INSUFFICIENCYAldosterone has a primary role in

promoting:Conservation of NaNa++

Secretion of KK++ by the nephrons of the kidney

Addison’s disease is characterized by aldosterone deficiencyThus the kidney is unable

to secrete potassium at anormal rate

65

OLIGURIC RENAL FAILUREOLIGURIC RENAL FAILURE

Kidney loses the ability to secrete K+

66

SPINOLACTONESPINOLACTONEDiuretic that is antagonistic to

the effects of aldosteroneCauses some rise in serum KK++

levels by interfering with KK++ secretion in the kidneys

Increases may not be significantBut individuals taking the

diuretic are at risk ifpotassium is administered

67

TREATMENTTREATMENT1) Counteract effects of KK++ ions at

the level of the cell membrane2) Promotion of KK++ ion movements

into cells3) Removal of KK++ ions from the

body

68

SALT INFUSIONSSALT INFUSIONS

Infusion of calcium gluconate calcium gluconate oror NaCl NaCl solutionsImmediately counteract the

effects of KK++ ions on the heartEffective for only 1-2 hours

69

SODIUM BICARBONATESODIUM BICARBONATE

NaHCONaHCO33 also reverses hyperkalemic effects on the heart

If acidosis is a factor also raises the pH of body fluids

70

INSULIN-GLUCOSE INSULIN-GLUCOSE INFUSIONINFUSION

Insulin given with glucoseEffective in about 30

minutes Has a duration of action

of up to 6 hours

Insulin promotes the shift of KK++ ions into cells

Glucose prevents insulin-induced hypoglycemia

71

KAYEXALATEKAYEXALATEKayexalate (cation exchange (cation exchange

resin)resin)Removes KK++ ions from the body by

exchanging KK++ for NaNa++

Exchange time is about 45 minutes

Effective for up to6 hours

72

DIALYSISDIALYSIS

Peritoneal dialysis or hemodialysisEffectively clears the blood of high

KK++ levels as well

73

CAUSES OF HYPERKALEMIACAUSES OF HYPERKALEMIA

CAUSE COMMENTS

hyperkalemic periodic paralysis inherited disorder in which there are suddenshifts of cellular K+ to extracellularcompartments

acidosis compensatory shift of H+ into cells in exchangefor movement of K+ to extracellularcompartments

burns cell destruction with release of K+

transfusion of blood that has beenstored

release of K+ from hemolyzed red blood cells

spironolactone diuretic that is an aldosterone antagonist;interferes with reabsorption of Na+ andsecretion of K+

too rapid intravenous infusion of KCl special risk of hyperkalemia if their isimpaired renal secretion of K+

use of K+ containing salt substitutes excessive ingestion

potassium salts of antibiotics additional source of K+

acute oliguric renal failure impaired secretion of K+

74

HYPOKALEMIAHYPOKALEMIA

Defined as a serum KK++ level that is below normal (< 3 meq / liter)(< 3 meq / liter)

Serum concentrations will decrease if:There is an intracellular flux of KK++

KK++ ions are lost from the gastrointestinal or urinary tract

KK++

75

ALKALOSISALKALOSISAlkalosisAlkalosis causes and is caused

by hypokalemiaAlkalosis is defined as a

decrease of hydrogen ions or an increase of bicarbonate in extracellular fluidsOpposite of acidosis

KK++

HH++

HCOHCO33--

76

ALKALOSISALKALOSISAlkalosis elicits a compensatory

response causing HH++ ions to shift from cells to extracellular fluidsThis corrects the acid-base

imbalance

HCOHCO33--HCOHCO33

--

HCOHCO33--

HCOHCO33--

HCOHCO33--

HCOHCO33--

HH++

HH++ HH++

HH++ HH++

HH++

HH++ HH++

77

ALKALOSISALKALOSISH+ ions are exchanged for KK++

(potassium moves into cells)Thus serum concentrations of KK++

are decreasedAnd alkalosis causes

hypokalemia

HCOHCO33--HCOHCO33

--

HCOHCO33--

HCOHCO33--

HCOHCO33--

HCOHCO33--

HH++

HH++ HH++

HH++ HH++

HH++

HH++ HH++

KK++KK++

KK++

KK++

KK++

KK++

KK++

KK++

78

ALKALOSISALKALOSISConversely when K+ ions are lost from

the cellular and extracellular compartmentsSodium and hydrogen ions enter cells

in a ratio of 2:1 as replacementThis loss of extracellular H+

causes alkalosis HCOHCO33--

HH++

KK++HCOHCO33

--

HCOHCO33--

HCOHCO33--

HCOHCO33--

HCOHCO33--

HCOHCO33--

HH++

HH++HH++

HH++HH++

HH++

NaNa++

KK++

KK++

KK++

KK++

KK++KK++

KK++ NaNa++

NaNa++

NaNa++

NaNa++

NaNa++

NaNa++

79

KIDNEY FUNCTIONKIDNEY FUNCTIONKidney function is altered by

hypokalemiaNaNa++ ions are reabsorbed into the blood

when KK++ ions are secreted into the urine by kidney tubules

K+

Tubular lumen

K+K+

K+

K+K+

K+

Na+

Na+

Na+

Na+

Na+

Na+

Na+

Peritubular fluid

NORMAL

80

KIDNEY FUNCTIONKIDNEY FUNCTIONKidney function is altered by

hypokalemiaIf adequate numbers of KK++ are not

available for this exchangeHH++ ions are secreted instead

H+

Tubular lumen

K+H+

K+

H+K+

H+

Na+

Na+

Na+

Na+

Na+

Na+

Na+

Peritubular fluid

HYPOKALEMIA

81

KIDNEY FUNCTIONKIDNEY FUNCTIONHypokalemia promotes renal loss

of HH++ ions and thus results in alkalosis

82

NORMAL NEPHRONNORMAL NEPHRONNormal nephron functionis to secrete H+ and K+ in exchange for Na+

capillary

distal tubule

H+

K+

Na+

Blood

Urine

83

NEPHRON ACTION IN NEPHRON ACTION IN HYPOKELEMIAHYPOKELEMIA

capillary

distal tubule

H+

K+

Na+

In HypokalemiaHypokalemia the kidneyselectively secretesHH++ ions in preference to KK++ ions

The loss of HH++ ions may lead to alkalosis

Blood

Urine

84

ALKALOSISALKALOSIS

capillary

distal tubule

H+

K+

Na+

retained

K+

excreted

1) in alkalosis there is a decrease in extracellular fluid HH++

2) the kidney retainshydrogen ions tocorrect the alkalosis

3) the kidney then eliminates KK++ ions which can lead to HypokalemiaHypokalemia

Blood

Urine

85

CAUSES OF HYPOKALEMIACAUSES OF HYPOKALEMIA

CAUSE COMMENTS aldosterone excess favors renal Na+ reabsorption and K+ secretion

diarrhea diarrheal fluid contains high amounts of K+

diuretics in general causes K+ loss

distal renal tubular acidosis

kidney tubule defect in which K+ are secreted, and H+ are retained by the body

hypokalemic periodic paralysis

cause unknown; periodic influx of K+ into cells

Bartter’s syndrome syndrome in which aldosterone is sometimes elevated; probably a renal tubular defect so that K+ are lost

86

TREATMENT OF TREATMENT OF HYPOKALEMIAHYPOKALEMIA

Replacement of K+ either by:Oral KK++ salt supplementsDietIntravenous administration

of KK++ salt solutionDiuretic (spinolactone)(spinolactone) if

renal loss is at work

87

CALCIUM HOMEOSTASISCALCIUM HOMEOSTASISCaCa++++ plays an important role in:

Muscle contractionNerve impulse transmissionHormone secretionBlood clotting

88

CALCIUM HOMEOSTASISCALCIUM HOMEOSTASISNormal range for serum calcium is

9 - 10.5 mg/dl (4.5 - 5.3 meq / liter)

The range for proper function has narrow limits

CaCa++

++

== 4.9 meq / 4.9 meq / literliter

89

VITAMIN DVITAMIN DVitamin DVitamin D is involved in

maintaining serum Ca++ levels

90

VITAMIN DVITAMIN DSource of vitamin

D is either dietary or is synthesized by the bodyCholesterol is

converted in the skin by exposure to sunlight into a precursor product which is converted to an active form of vitamin D by the liver and kidneys

91

VITAMIN DVITAMIN DVitamin D enhances serum Ca++ levels

by:1)1) Directly promoting bone resorption with

the release of chemical salts2)2) Potentiating the effects of

parathormone (PTH)parathormone (PTH) on bone reabsorption3)3) Increasing absorption of CaCa++++ ions from

the intestine4)4) Reabsorption by the

kidney tubules

92

PARATHORMONEPARATHORMONESecreted into the bloodstream

by the parathyroid glandsEssential part of the Ca++

homeostatic mechanisms

93

PARATHORMONE ACTIONPARATHORMONE ACTIONPTH

1)1) Increases calcium ion absorption from the intestine Enhances the synthesis of the active form of vitamin D

2)2) Favors reabsorption of calcium

94

PARATHORMONE ACTIONPARATHORMONE ACTION

PTH 3)3) Favors excretion of phosphate

(POPO44 -3-3) by kidney tubules

4)4) Enhances bonereabsorption withthe release of CaCa++++

95

PARATHORMONE PARATHORMONE SECRETIONSECRETION

PTH secretion is:StimulatedStimulated by decreased

serum level of CaCa++++

InhibitedInhibited by increased serum levels of CaCa++++

PTPTHH

CaCa++

++

PTPTHH

CaCa++

++

96

CALCITONINCALCITONINCalcitonin is a hormone

secreted by the thyroid glandthyroid glandEffects of calcitonin are weak

compared to PTH

97

Rising blood Ca++ levels

CALCITONINCALCITONINDecreases serum Ca++ level by:

1)1) Interfering with bone resorption 2)2) Favoring bone uptake of calcium 3)3) Promoting excretion of calcium by

the kidney

Parathyroid glands release PTH

Calcitonin stimulates calcium salt deposit in bone

Thyroid gland releases calcitonin

CALCITONICALCITONINN

Falling blood Ca++ levels

Osteoclasts degrade bone and release Ca++

PTHPTH

98

STORES OF CALCIUMSTORES OF CALCIUM

bone calciumbone calcium

intracellularintracellularcalciumcalcium

extracellularextracellularcalciumcalcium

renal excretionrenal excretion

absorption fromabsorption fromintestineintestine

There are exchangeable stores of calcium in bone and in cells. This total pool is in equilibrium with calcium in extracellular fluid. Serum calcium levels are also maintained by a balance between renal excretion and intestinal absorption

99

HYPERCALCEMIAHYPERCALCEMIAA serum calcium level of 10.5

mg / dl or above results in hypercalcemia

CaCa++

++

CaCa++

++

HypercalceHypercalcemiamia

10.10.55

==

HypocalcemiHypocalcemiaa

9.09.0 ==

100

HYPERCALCEMIAHYPERCALCEMIAHighHigh levels of Ca++:

Interfere with nerve impulseInterfere with muscle contractionMay cause kidney stonesMay precipitate out of body

tissues (at high levels)

101

CAUSES FOR CAUSES FOR HYPERCALCEMIAHYPERCALCEMIA

1)1) Overactive parathyroid glands2)2) Hyperthyroidism increases

bone resorption 3)3) Large doses of vitamin D

102

CAUSES FOR CAUSES FOR HYPERCALCEMIAHYPERCALCEMIA

4)4) Confinement to bed for weeks at a timeBone reabsorption occurs at a more

rapid rate than bone formation5)5) Some malignancies secrete

hormones that cause bone resorption

103

CAUSES FOR CAUSES FOR HYPERCALCEMIAHYPERCALCEMIA6)6) Milk-alkali syndrome

Excessive and prolonged ingestion of milk and alkaline antacids (peptic ulcer)

Sodium bicarbonate and calcium carbonate used as antacids

Metabolic acidosis results because of increased levels of plasma bicarbonate

104

MILK-ALKALI SYNDROMEMILK-ALKALI SYNDROMEAlkalosis promotes hypercalcemia

1)1) Causes increased kidney resorption of calcium

2)2) Decreases the capacity of bone to take up additional calcium

105

CAUSES OF HYPERCALCEMIACAUSES OF HYPERCALCEMIA

CAUSE COMMENTS vitamin D excess promotes calcium absorption from

intestine, reabsorption from kidney hyperparathyroidism excessive production of PTH hyperthyroidism causes mild hypercalcemia; causes bone

resorption thiazide diuretics cause small increases in serum calcium

in normal individuals; increased renal reabsorption

excessive and prolonged ingestion of milk and antacids

alkalosis causes hypercalcemia

some malignancies probably secretion of PTH - like substances by malignancies

immobilization patients who are confined to bed; bone resorption

106

TREATMENTTREATMENTIntravenous or oral

administration of phosphatephosphate decreases plasma calcium levels by interfering with bone resorption

CalcitoninCalcitonin reduces activities of bone destroying cells (osteoclasts)

GlucocorticoidsGlucocorticoids inhibit intestinal absorption of calcium

107

TREATMENTTREATMENTSome diureticsdiuretics promote

excretion of calcium by the kidneys

Infusion of saline saline (NaCl)(NaCl) or sodiumsodium sulfate sulfate (Na(Na22SOSO44)) increases urinary calcium excretion

108

HYPOCALCEMIAHYPOCALCEMIADefined as a lowlow serum calcium level

Less than 9 mg / dl

CaCa++

++

CaCa++

++

HypercalceHypercalcemiamia

10.10.55

==

HypocalcemiHypocalcemiaa

9.09.0 ==

109

HYPOCALCEMIAHYPOCALCEMIAPhysiological response to low

calcium serum levelsIncreased secretion of PTH

Which increases calcium by favoring bone resorptionIntestinal absorptionRenal reabsorption

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CAUSES FOR CAUSES FOR HYPOCALCEMIAHYPOCALCEMIA

1) Inadequate vitamin D1) Inadequate vitamin Da)a) Nutritional deficienciesb)b) Impaired intestinal absorption

ex: partial gastrectomyc)c) Liver or kidney dysfunction

interferes with formation of active form of vitamin D

111

CAUSES FOR HYPOCALCEMIACAUSES FOR HYPOCALCEMIAd)d) Inadequate exposure to sunlight

Reduction in formation of active vitamin D in the skin

e)e) Intestinal or bone unresponsiveness to action of vitamin D

112

CAUSES FOR CAUSES FOR HYPOCALCEMIAHYPOCALCEMIA2) Loss of parathyroid glands or 2) Loss of parathyroid glands or

loss of functionloss of function3) Pancreatitis3) Pancreatitis

Defect in PTH secretionCalcium deposits form in soft tissues

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CAUSES FOR CAUSES FOR HYPOCALCEMIAHYPOCALCEMIA

4) Renal failure4) Renal failureReduction in the formation of an

active vitamin D metaboliteAltered bone response to PTH is also

a factor

114

CAUSES OF CAUSES OF HYPOCALCEMIAHYPOCALCEMIA

CAUSE COMMENTS hypoparathyroidism may be caused by surgical

procedures involving the neck; PTH deficiency

DiGeorge’s syndrome congenital absence of parathyroid glands

multiple endocrine deficiency-autoimmune-candidasis syndrome

inherited condition in which hypoparathyroidism is present

vitamin D deficiency decreased absorption of calcium from intestines

115

TREATMENTTREATMENT

Calcium salts administered intravenously or orallyCalcium gluconate or calcium

chloride solutionsVitamin D may be given

116

END OFEND OFFLUID AND FLUID AND

ELECTROLYTES PART 2ELECTROLYTES PART 2

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1 ADVANCED PHYSIOLOGY FLUID & ELECTROLYTES PART 2 Instructor Terry Wiseth