1
ADVANCED ADVANCED PHYSIOLOGYPHYSIOLOGY
FLUID & ELECTROLYTESFLUID & ELECTROLYTES
PART 2PART 2
Instructor Terry WisethInstructor Terry Wiseth
NORTHLAND COLLEGENORTHLAND COLLEGE
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++
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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++
Click to seeanimation
6
ELECTROLYTE BALANCEELECTROLYTE BALANCEAldosterone, ANP and ADH regulate
sodium levels within the body, while 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--
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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
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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+
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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 In the CNS tight junctions exist between endothelial cells of the between endothelial cells of the capillary wallscapillary walls
These junctions restrict diffusion These junctions restrict diffusion from capillaries to the from capillaries to the interstitium of the braininterstitium of the brainblood-brain barrierblood-brain barrier
Increased levels of sodium ions Increased levels of sodium ions in the blood does not result in in the blood does not result in increased sodium ions in brain increased sodium ions in brain interstitial fluidinterstitial fluid
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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
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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
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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
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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)
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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
Click to animate
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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
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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
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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
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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
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TREATMENT OF TREATMENT OF HYPERNATREMIAHYPERNATREMIA
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
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TREATMENT OF TREATMENT OF HYPERNATREMIAHYPERNATREMIA
Treatment is best handled by giving slow infusions of glucose solutions
This dilutes high plasmasodium ion concentrations
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TREATMENT OF TREATMENT OF HYPERNATREMIAHYPERNATREMIA
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
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GENERAL RESPONSE TO GENERAL RESPONSE TO HYPONATREMIAHYPONATREMIA
Suppression of thirst
Suppression of ADH secretion
Both favor decreasing wateringestion and increasingurinary output
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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
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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
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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
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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
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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
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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
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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
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POTASSIUM ION POTASSIUM ION LOSSLOSS
KK++
NaNa++
KK++KK
++ KK++
PlasmaPlasmaInterstitial fluidInterstitial fluid
CellCell
KK++
KK++
NaNa++
NaNa++
Click to seeanimation
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DILUTIONAL EFFECTDILUTIONAL EFFECT5) 5) Diuretic therapyDiuretic therapy
Common cause of hyponatremia
Loss of sodium and potassium often occurs in addition to fluid loss
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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
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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+
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HYPERKALEMIAHYPERKALEMIANormal Normal serumserum potassium level potassium level
(3-5 meq / liter)(3-5 meq / liter)As compared to As compared to NaNa++ (142 meq / liter) (142 meq / liter)
IntracellularIntracellular levels of potassium levels of potassium(140-150 meq / liter)(140-150 meq / liter)This high intracellular level is This high intracellular level is
maintained by active transport by the maintained by active transport by the sodium-potassium pumpsodium-potassium pump
K+
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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+
45
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+
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HYPERKALEMIAHYPERKALEMIAWhen hyperkalemia develops When hyperkalemia develops
potassium ions diffuse potassium ions diffuse intointo the cell the cellThis causes a movement of This causes a movement of HH++ ions ions outout
of the cell to maintain a neutral of the cell to maintain a neutral electrical balanceelectrical balance
As a result the physiological As a result the physiological response to hyperkalemia causes response to hyperkalemia causes acidosisacidosis
K+
K+
K+
K+
K+
K+H+
H+
H+
H+
H+H+
H+H+
H+
HYPERKALEMIA
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HYPERKALEMIAHYPERKALEMIAThe reverse occurs as wellThe reverse occurs as wellThe body is protected from harmful The body is protected from harmful
effects of an increase in effects of an increase in extracellular Hextracellular H++ ions (acidosis) ions (acidosis) HH++ ions inside the cells are tied up by ions inside the cells are tied up by
proteins (proteins (PrPr --))This causes a shift of potassium This causes a shift of potassium
ions out of the cellsions out of the cells
H+
H+
H+
H+
H+
H+H+
H+
H+
K+
K+K+
K+K+
K+
ACIDOSIS
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HYPERKALEMIAHYPERKALEMIASummarized:
Hyperkalemia causes acidosis Acidosis causes hyperkalemia
HYPERKALEMIAH+
H+
H+
H+
H+
H+
H+ H+
K+
K+
K+
K+
K+
K+
K+ K+
ACIDOSIS
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HYPERKALEMIAHYPERKALEMIASummarized:
Hyperkalemia causes acidosis Acidosis causes hyperkalemia
HYPERKALEMIAH+
H+
H+
H+
H+
H+
H+ H+
K+
K+
K+
K+
K+
K+
K+ K+
ACIDOSIS
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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
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CAUSES FOR CAUSES FOR HYPERKALEMIAHYPERKALEMIA
1) Increased input of potassium
2) Impaired excretion of potassium
3) Impaired uptake of potassium by cells
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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
53
CELLULAR-EXTRACELLULAR CELLULAR-EXTRACELLULAR SHIFTSSHIFTSInsulin deficiency predisposes
an individual to hyperkalemiaCellular 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
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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+
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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
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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
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OLIGURIC RENAL FAILUREOLIGURIC RENAL FAILURE
Kidney loses the ability to secrete K+
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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
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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
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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
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SODIUM BICARBONATESODIUM BICARBONATE
NaHCONaHCO33 also reverses hyperkalemic effects on the heart
If acidosis is a factor also raises the pH of body fluids
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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
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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
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DIALYSISDIALYSIS
Peritoneal dialysis or hemodialysisEffectively clears the blood of high
KK++ levels as well
65
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+
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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++
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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--
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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++
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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++
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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++
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KIDNEY FUNCTIONKIDNEY FUNCTIONKidney function is altered by hypokalemia
NaNa++ 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
72
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
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KIDNEY FUNCTIONKIDNEY FUNCTIONHypokalemia promotes renal loss
of HH++ ions and thus results in alkalosis
74
NORMAL NEPHRONNORMAL NEPHRONNormal nephron functionis to secrete H+ and K+ in exchange for Na+
capillary
distal tubule
H+
K+
Na+
Blood
Urine
75
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
76
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
77
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
78
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
79
CALCIUM HOMEOSTASISCALCIUM HOMEOSTASISCaCa++++ plays an important role in:
Muscle contractionNerve impulse transmissionHormone secretionBlood clotting
80
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
81
VITAMIN DVITAMIN DVitamin DVitamin D is involved in
maintaining serum Ca++ levels
82
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
83
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
84
PARATHORMONEPARATHORMONESecreted into the bloodstream
by the parathyroid glandsEssential part of the Ca++
homeostatic mechanisms
85
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
86
PARATHORMONE ACTIONPARATHORMONE ACTION
PTH 3)3) Favors excretion of phosphate (POPO44
-3-3) by kidney tubules4)4) Enhances bone
reabsorption withthe release of CaCa++++
87
PARATHORMONE PARATHORMONE SECRETIONSECRETION
PTH secretion is:StimulatedStimulated by decreased
serum level of CaCa++++
InhibitedInhibited by increased serum levels of CaCa++++
PTPTHH
CaCa++
++
PTPTHH
CaCa++
++
88
CALCITONINCALCITONINCalcitonin is a hormone
secreted by the thyroid glandthyroid glandEffects of calcitonin are weak
compared to PTH
89
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
Falling blood Ca++ levels
Osteoclasts degrade bone and release Ca++
PTHPTH
CALCITONICALCITONINN
90
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
91
HYPERCALCEMIAHYPERCALCEMIAA serum calcium level of 10.5
mg / dl or above results in hypercalcemia
CaCa++
++
CaCa++
++
HypercalcemHypercalcemiaia
10.10.55
==
HypocalcemiHypocalcemiaa
9.09.0 ==
92
HYPERCALCEMIAHYPERCALCEMIAHighHigh levels of Ca++:
Interfere with nerve impulseInterfere with muscle contractionMay cause kidney stonesMay precipitate out of body
tissues (at high levels)
93
CAUSES FOR CAUSES FOR HYPERCALCEMIAHYPERCALCEMIA
1)1) Overactive parathyroid glands2)2) Hyperthyroidism increases
bone resorption 3)3) Large doses of vitamin D
94
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
95
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
96
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
97
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
98
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
99
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
100
HYPOCALCEMIAHYPOCALCEMIADefined as a lowlow serum calcium level
Less than 9 mg / dl
CaCa++
++
CaCa++
++
HypercalcemHypercalcemiaia
10.10.55
==
HypocalcemiHypocalcemiaa
9.09.0 ==
101
HYPOCALCEMIAHYPOCALCEMIAPhysiological response to low
calcium serum levelsIncreased secretion of PTH
Which increases calcium by favoring bone resorptionIntestinal absorptionRenal reabsorption
102
CAUSES FOR HYPOCALCEMIACAUSES FOR HYPOCALCEMIA1) Inadequate vitamin D1) Inadequate vitamin D
a)a) Nutritional deficienciesb)b) Impaired intestinal absorption
ex: partial gastrectomyc)c) Liver or kidney dysfunction
interferes with formation of active form of vitamin D
103
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 ofvitamin D
104
CAUSES FOR HYPOCALCEMIACAUSES FOR HYPOCALCEMIA2) 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
105
CAUSES FOR HYPOCALCEMIACAUSES FOR HYPOCALCEMIA4) Renal failure4) Renal failure
Reduction in the formation of an active vitamin D metabolite
Altered bone response to PTH is also a factor
106
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
107
TREATMENTTREATMENT
Calcium salts administered intravenously or orallyCalcium gluconate or calcium
chloride solutionsVitamin D may be given
108
END OFEND OFFLUID AND FLUID AND
ELECTROLYTES PART 2ELECTROLYTES PART 2
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