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ADVANCED PHYSIOLOGY FLUID & ELECTROLYTES PART 2 Instructor Terry Wiseth. NORTHLAND COLLEGE. ELECTROLYTE BALANCE. The exchange of interstitial and intracellular fluid is controlled mainly by the presence of the electrolytes sodium and potassium. Na +. K +. K +. Na +. Na +. Na +. K +. K +.

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ADVANCED PHYSIOLOGY FLUID & ELECTROLYTES PART 2 Instructor Terry Wiseth

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Advanced physiology fluid electrolytes part 2 instructor terry wiseth l.jpg

ADVANCED PHYSIOLOGYFLUID & ELECTROLYTESPART 2Instructor Terry Wiseth

NORTHLAND COLLEGE


Electrolyte balance l.jpg

ELECTROLYTE BALANCE

  • The exchange of interstitial and intracellular fluid is controlled mainly by the presence of the electrolytes sodium and potassium

Na+

K+

K+

Na+

Na+

Na+

K+

K+


Electrolyte balance3 l.jpg

ELECTROLYTE BALANCE

  • Potassium 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

K+

Na+


Electrolyte balance4 l.jpg

ELECTROLYTE BALANCE

  • A 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

Click to seeanimation

Na+

K+

K+

H2O

H2O

Na+

H2O

H2O

K+

Na+

Na+

K+

H2O

H2O

H2O

H2O


Electrolyte balance5 l.jpg

ELECTROLYTE BALANCE

  • A 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

Click to seeanimation

Na+

K+

K+

H2O

Na+

H2O

H2O

H2O

Na+

K+

Na+

K+

H2O

H2O

H2O

H2O


Electrolyte balance6 l.jpg

ELECTROLYTE BALANCE

  • Aldosterone, ANP and ADH regulate sodium levels within the body, while aldosterone can be said to regulate potassium

Na+

ADH

ANP

K+

aldosterone


Electrolyte balance7 l.jpg

ELECTROLYTE BALANCE

Na+

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

  • Anions which accompany sodium are chloride (Cl-) and bicarbonate (HCO3-)

  • Considered an indicator of total solute concentration of plasma osmolality

Cl-

HCO3-


Electrolyte balance8 l.jpg

ELECTROLYTE BALANCE

  • Sodium ions are osmotically important in determining water movements

  • A discussion of sodium must also include

    • Chlorine

    • Bicarbonate

    • Hydrogen ions

  • Potassium and calcium serum concentrations are also important electrolytes in the living system

H2O

H2O

H2O

H2O

H2O

H2O

H2O

H2O

H2O

H2O

H2O

H2O

H2O

H2O

H2O


Electrolyte balances l.jpg

ELECTROLYTE BALANCES

  • Hypernatremia - elevated sodium levels

  • Hyponatremia -- lowered sodium levels

  • Hyperkalemia -- elevated potassium levels

  • Hypokalemia ---- lowered potassium levels

Click

  • Hypercalcemia - elevated calcium levels

  • Hypokalcemia -- lowered calcium levels

Click


Hypernatremia l.jpg

HYPERNATREMIA

  • Normal range for blood levels of sodium is app. 137 - 143 meq/liter

  • Hypernatremia 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 principles l.jpg

SODIUM PRINCIPLES

  • 1) Sodium ions do not cross cell membranes as quickly as water does

H2O

H2O

H2O

H2O

H2O

Na+

Na+


Sodium principles12 l.jpg

SODIUM PRINCIPLES

  • 2) Cells pump sodium ions out of the cell by using sodium-potassium pumps

Na+

Na+

Na+

Na+


Sodium principles13 l.jpg

SODIUM PRINCIPLES

  • 3) 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+


Results of hypernatremia l.jpg

RESULTS OF HYPERNATREMIA

  • 1) Water is osmotically drawn out of the cells

    • Resulting in dehydration

  • 2) Increase in extracellular fluid volume

Intracellular

fluid

volume

Extracellular

fluid

volume


Cns reaction to hypernatremia l.jpg

CNS REACTION TO HYPERNATREMIA

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

  • These junctions restrict diffusion from capillaries to the interstitium of the brain

    • blood-brain barrier

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


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CNS REACTION TO HYPERNATREMIA

  • As the result of an osmotic gradient, water shifts from the interstitium and cells of the brain and enters the capillaries

    • The brain tends to shrink and the capillaries dilate and possibly rupture

    • Result is cerebral hemorrhage, blood clots, and neurological dysfunction

H2O


Cns protective mechanism l.jpg

CNS PROTECTIVE MECHANISM

  • 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 MECHANISM

  • Idiogenic osmoles accumulate inside brain cells

    • K+, 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

H2O


Causes of hypernatremia l.jpg

CAUSES OF HYPERNATREMIA

  • 1) Water loss

  • 2) Sodium ion overload

    • Most 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


Water loss l.jpg

WATER LOSS

  • Diabetes insipidus caused by inadequate ADH or renal insensitivity to ADH results in large urinary fluid loss

    • Increased fluid loss also occurs as the result of osmotic diuresis (high solute loads are delivered to the kidney for elimination)


Water loss21 l.jpg

WATER LOSS

  • Diabetes 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

H2O

H2O

H2O

Glucose

Glucose

Glucose

H2O

Glucose

H2O

Click to animate

H2O

Glucose

Glucose

H2O

H2O

Glucose

Glucose

H2O

H2O

Glucose

Glucose

H2O

H2O

Glucose


Water loss22 l.jpg

WATER LOSS

  • High 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


Sodium excess l.jpg

SODIUM EXCESS

  • Occurs less frequently than water loss

  • Retention or intake of excess sodium

    • ex: IV infusion of hypertonic sodium ion solutions

  • Aldosterone promotes sodium and water retention by the kidney

    • High levels of aldosterone may result in mild hypernatremia


Causes of hypernatremia24 l.jpg

CAUSES OF HYPERNATREMIA


Treatment of hypernatremia l.jpg

TREATMENT OF HYPERNATREMIA

  • Re-hydration is the primary objective in most cases

    • Decreases sodium concentrations

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


Treatment of hypernatremia26 l.jpg

TREATMENT OF HYPERNATREMIA

  • 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


Treatment of hypernatremia27 l.jpg

TREATMENT OF HYPERNATREMIA

  • Treatment is best handled by giving slow infusions of glucose solutions

    • This dilutes high plasmasodium ion concentrations


Treatment of hypernatremia28 l.jpg

TREATMENT OF HYPERNATREMIA

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

  • Diuretics can be used to induce sodium and water diuresis

    • However if kidney function is not normal peritoneal dialysis may be required


Hyponatremia l.jpg

HYPONATREMIA

  • 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

Na+


Cns response to hyponatremia l.jpg

CNS RESPONSE TO HYPONATREMIA

  • 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


General response to hyponatremia l.jpg

GENERAL RESPONSE TO HYPONATREMIA

  • Suppression of thirst

  • Suppression of ADH secretion

    • Both favor decreasing wateringestion and increasingurinary output


Symptoms of hyponatremia l.jpg

SYMPTOMS OF HYPONATREMIA

  • Primarily neurological (net flux of water into the brain)

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

  • Sodium ion levels of less than 110meq / liter bring on seizures and coma


Hyponatremia33 l.jpg

H O

2

HYPONATREMIA

Na+

  • Produced by:

    • 1) A loss of sodium ions

    • 2) Water excess

      • Water excess can be due to:

        • Ingestion

        • Renal retention


Dilutional effect l.jpg

DILUTIONAL EFFECT

  • 1) Isotonic fluid loss

  • 2) Antidiuretic hormone secretion

  • 3) Acute or chronic renal failure

  • 4) Potassium ion loss

  • 5) Diuretic therapy

H2O

H2O

H2O

Na+

Na+

H2O

H2O

H2O

H2O

Na+

H2O

H2O

H2O

H2O

H2O

H2O

Na+

Na+

Na+

Na+

H2O

H2O

H2O

H2O

H2O

H2O

Na+


Dilutional effect35 l.jpg

DILUTIONAL EFFECT

  • 1) Isotonic fluid loss

    • Burns, fever, hemorrhage

    • Indirect cause of hyponatremia

    • Any volume loss stimulates thirst and leads to increased water ingestion

      • Thus isotonic fluid loss can cause hyponatremia not because of sodium loss but because of increased water intake


Dilutional effect36 l.jpg

DILUTIONAL EFFECT

  • 2) Antidiuretic hormone secretion

    • Enhances water retention

  • 3) Acute or chronic renal failure

    • The kidney fails to excrete water

    • Can lead to hyponatremia


Dilutional effect37 l.jpg

DILUTIONAL EFFECT

  • 4) Potassium 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


Potassium ion loss l.jpg

1) extracellular

potassium loss

3) intracellular electrical balance

is maintained by diffusion of

sodium ions into cells

2) diffusion of potassium

ions into extracellular

compartments

POTASSIUM ION LOSS

K+

Na+

Na+

cell

K+

K+

K+

interstitial fluid

plasma


Potassium ion loss39 l.jpg

POTASSIUM ION LOSS

Na+

Na+

K+

Cell

Na+

K+

K+

Click to seeanimation

K+

K+

K+

Interstitial fluid

Plasma


Dilutional effect40 l.jpg

DILUTIONAL EFFECT

  • 5) Diuretic therapy

    • Common cause of hyponatremia

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


Causes of hyponatremia l.jpg

CAUSES OF HYPONATREMIA


Reactions to hyponatremia l.jpg

REACTIONS TO HYPONATREMIA

Increased ADHrelease

Increased Thirst

Decreased urinary H2O loss

Increased H2O gain

Osmoreceptorsstimulated

Click to viewincreased Na+

Increased Na+

Additional H2Odilutes Na+

HomeostasisNormal Na+

H2O lossconcentrates Na+

Decreased Na+

Click to viewdecreased Na+

Decreased ADHrelease

Decreased Thirst

Increased urinary H2O loss

Decreased H2O gain

Osmoreceptorsinhibited


Hyperkalemia l.jpg

HYPERKALEMIA

  • Normal serum potassium level(3-5 meq / liter)

    • As compared to Na+ (142 meq / liter)

  • Intracellular levels of potassium(140-150 meq / liter)

    • This high intracellular level is maintained by active transport by the sodium-potassium pump

K+


Na k pump l.jpg

Na+ / K+ Pump

  • Cells pump K+ ions in and Na+ ions out of the cell by using sodium-potassium pumps

K+

K+

Na+

K+

K+

Na+

Na+

Na+


Hyperkalemia45 l.jpg

HYPERKALEMIA

  • Hyperkalemia is an elevated serum potassium (K+) ion level

  • A consequence of hyperkalemia is acidosis

    • an increase in H+ ions in body fluids

  • Changes in either K+ or H+ ion levels causes a compartmental shift of the other

K+


Hyperkalemia46 l.jpg

HYPERKALEMIA

  • When hyperkalemia develops potassium ions diffuse into the cell

    • This causes a movement of H+ ions out of the cell to maintain a neutral electrical balance

  • As a result the physiological response to hyperkalemia causes acidosis

H+

K+

HYPERKALEMIA

H+

K+

H+

K+

H+

K+

H+

H+

K+

H+

H+

K+

H+


Hyperkalemia47 l.jpg

HYPERKALEMIA

  • The reverse occurs as well

  • The body is protected from harmful effects of an increase in extracellular H+ ions (acidosis)

    • H+ ions inside the cells are tied up by proteins (Pr-)

  • This causes a shift of potassium ions out of the cells

H+

H+

ACIDOSIS

K+

H+

K+

H+

K+

H+

K+

H+

H+

K+

H+

H+

K+


Hyperkalemia48 l.jpg

H+

H+

H+

H+

K+

K+

H+

K+

K+

H+

H+

K+

H+

K+

K+

K+

HYPERKALEMIA

  • Summarized:

    • Hyperkalemia causes acidosis

    • Acidosis causes hyperkalemia

HYPERKALEMIA

ACIDOSIS


Hyperkalemia49 l.jpg

H+

H+

H+

H+

K+

K+

H+

K+

K+

H+

H+

K+

H+

K+

K+

K+

HYPERKALEMIA

  • Summarized:

    • Hyperkalemia causes acidosis

    • Acidosis causes hyperkalemia

HYPERKALEMIA

ACIDOSIS


Symptoms of hyperkalemia l.jpg

SYMPTOMS OF HYPERKALEMIA

  • Muscle contraction is affected by changes in potassium levels

  • Hyperkalemia blocks the transmission of nerve impulses along muscle fibers

    • Causes muscle weakness and paralysis

  • Can cause arrhythmia's and heart conduction disturbances


Causes for hyperkalemia l.jpg

CAUSES FOR HYPERKALEMIA

  • 1) Increased input of potassium

  • 2) Impaired excretion of potassium

  • 3) Impaired uptake of potassium by cells


Increased input l.jpg

INCREASED INPUT

  • A) Intravenous KCl infusion

  • B) Use of K+ containing salt substitutes

  • C) Hemolysis of RBC during blood transfusions with release of K+

  • D) Damaged and dying cells release K+

    • Burns, crush injuries, ischemia

  • E) Increased fragility of RBC


Cellular extracellular shifts l.jpg

Insulin

CELLULAR-EXTRACELLULAR SHIFTS

  • Insulin deficiency predisposes an individual to hyperkalemia

  • Cellular uptake of K+ ions is enhanced by insulin, aldosterone and epinephrine

    • Provides protection from extracellular K+ overload

K+

K+

K+

K+

K+

Click to viewanimation

K+


Cellular extracellular shifts54 l.jpg

CELLULAR-EXTRACELLULAR SHIFTS

  • 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+


Hyperkalemic periodic paralysis l.jpg

HYPERKALEMIC PERIODIC PARALYSIS

  • Inherited disorder in which serum K+ level rise periodically

    • Caused by a shift of K+ from muscle to blood in response to ingestion of potassium or exercise

    • Reasons for the shift arenot clear

  • Attacks are characterizedby muscle weakness


Renal insufficiency l.jpg

RENAL INSUFFICIENCY

  • Aldosterone has a primary role in promoting:

    • Conservation of Na+

    • Secretion of K+ by the nephrons of the kidney

  • Addison’s disease is characterized by aldosterone deficiency

    • Thus the kidney is unableto secrete potassium at anormal rate


Oliguric renal failure l.jpg

OLIGURIC RENAL FAILURE

  • Kidney loses the ability to secrete K+


Spinolactone l.jpg

SPINOLACTONE

  • Diuretic that is antagonistic to the effects of aldosterone

    • Causes some rise in serum K+ levels by interfering with K+ secretion in the kidneys

  • Increases may not be significant

    • But individuals taking thediuretic are at risk ifpotassium is administered


Treatment l.jpg

TREATMENT

  • 1) Counteract effects of K+ ions at the level of the cell membrane

  • 2) Promotion of K+ ion movements into cells

  • 3) Removal of K+ ions from the body


Salt infusions l.jpg

SALT INFUSIONS

  • Infusion of calcium gluconate or NaCl solutions

    • Immediately counteract the effects of K+ ions on the heart

    • Effective for only 1-2 hours


Sodium bicarbonate l.jpg

SODIUM BICARBONATE

  • NaHCO3 also reverses hyperkalemic effects on the heart

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


Insulin glucose infusion l.jpg

INSULIN-GLUCOSE INFUSION

  • Insulin given with glucose

    • Effective in about 30 minutes

    • Has a duration of action of up to 6 hours

  • Insulin promotes the shift of K+ ions into cells

  • Glucose prevents insulin-induced hypoglycemia


Kayexalate l.jpg

KAYEXALATE

  • Kayexalate (cation exchange resin)

    • Removes K+ ions from the body by exchanging K+ for Na+

      • Exchange time is about 45 minutes

      • Effective for up to6 hours


Dialysis l.jpg

DIALYSIS

  • Peritoneal dialysis or hemodialysis

  • Effectively clears the blood of high K+ levels as well


Causes of hyperkalemia l.jpg

CAUSES OF HYPERKALEMIA


Hypokalemia l.jpg

HYPOKALEMIA

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

  • Serum concentrations will decrease if:

    • There is an intracellular flux of K+

    • K+ ions are lost from the gastrointestinal or urinary tract

K+


Alkalosis l.jpg

ALKALOSIS

  • Alkalosis causes and is caused by hypokalemia

  • Alkalosis is defined as a decrease of hydrogen ions or an increase of bicarbonate in extracellular fluids

    • Opposite of acidosis

H+

K+

HCO3-


Alkalosis68 l.jpg

ALKALOSIS

  • Alkalosis elicits a compensatory response causing H+ ions to shift from cells to extracellular fluids

    • This corrects the acid-baseimbalance

HCO3-

HCO3-

HCO3-

HCO3-

H+

H+

H+

HCO3-

H+

H+

H+

HCO3-

H+

H+


Alkalosis69 l.jpg

ALKALOSIS

  • H+ ions are exchanged for K+ (potassium moves into cells)

    • Thus serum concentrations of K+ are decreased

      • And alkalosis causeshypokalemia

HCO3-

HCO3-

HCO3-

K+

K+

K+

HCO3-

H+

K+

H+

K+

H+

K+

HCO3-

H+

H+

H+

HCO3-

K+

H+

H+

K+


Alkalosis70 l.jpg

ALKALOSIS

  • Conversely when K+ ions are lost from the cellular and extracellular compartments

    • Sodium and hydrogen ions enter cellsin a ratio of 2:1 as replacement

  • This loss of extracellular H+causes alkalosis

HCO3-

HCO3-

H+

H+

H+

HCO3-

HCO3-

Na+

Na+

H+

H+

Na+

HCO3-

K+

K+

H+

Na+

HCO3-

K+

K+

Na+

HCO3-

Na+

K+

H+

K+

Na+

K+

K+


Kidney function l.jpg

KIDNEY FUNCTION

  • Kidney function is altered by hypokalemia

    • Na+ ions are reabsorbed into the blood when K+ ions are secreted into the urine by kidney tubules

NORMAL

Peritubular fluid

Tubular lumen

K+

Na+

K+

Na+

Na+

K+

Na+

K+

K+

Na+

Na+

Na+

K+

K+


Kidney function72 l.jpg

KIDNEY FUNCTION

  • Kidney function is altered by hypokalemia

    • If adequate numbers of K+ are not available for this exchange

      • H+ ions are secreted instead

HYPOKALEMIA

Peritubular fluid

Tubular lumen

H+

Na+

K+

Na+

Na+

K+

Na+

H+

H+

Na+

Na+

Na+

H+

K+


Kidney function73 l.jpg

KIDNEY FUNCTION

  • Hypokalemia promotes renal loss of H+ ions and thus results in alkalosis


Normal nephron l.jpg

H+

K+

Na+

distal tubule

capillary

NORMAL NEPHRON

Normal nephron function

is to secrete H+ and K+ in

exchange for Na+

Blood

Urine


Nephron action in hypokelemia l.jpg

NEPHRON ACTION IN HYPOKELEMIA

In Hypokalemia the kidney

selectively secretes

H+ ions in preference

to K+ ions

The loss of H+ ions

may lead to alkalosis

H+

K+

Na+

distal tubule

capillary

Blood

Urine


Alkalosis76 l.jpg

ALKALOSIS

3) the kidney then eliminates K+ ions which can lead to Hypokalemia

1) in alkalosis there is a

decrease in extracellular

fluid H+

H+

retained

K+

K+

Na+

excreted

distal tubule

capillary

Blood

2) the kidney retains

hydrogen ions to

correct the alkalosis

Urine


Causes of hypokalemia l.jpg

CAUSES OF HYPOKALEMIA


Treatment of hypokalemia l.jpg

TREATMENT OF HYPOKALEMIA

  • Replacement of K+ either by:

    • Oral K+ salt supplements

    • Diet

    • Intravenous administration of K+ salt solution

    • Diuretic (spinolactone) if renal loss is at work


Calcium homeostasis l.jpg

CALCIUM HOMEOSTASIS

  • Ca++ plays an important role in:

    • Muscle contraction

    • Nerve impulse transmission

    • Hormone secretion

    • Blood clotting


Calcium homeostasis80 l.jpg

CALCIUM HOMEOSTASIS

  • Normal range for serum calcium is 9 - 10.5 mg/dl (4.5 - 5.3 meq / liter)

  • The range for proper function has narrow limits

Ca++

=

4.9 meq / liter


Vitamin d l.jpg

VITAMIN D

  • Vitamin D is involved in maintaining serum Ca++ levels


Vitamin d82 l.jpg

VITAMIN D

  • Source of vitamin D is either dietary or is synthesized by the body

    • Cholesterol 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


Vitamin d83 l.jpg

VITAMIN D

  • Vitamin D enhances serum Ca++ levels by:

    • 1) Directly promoting bone resorption with the release of chemical salts

    • 2) Potentiating the effects of parathormone (PTH) on bone reabsorption

    • 3) Increasing absorption of Ca++ ions from the intestine

    • 4) Reabsorption by thekidney tubules


Parathormone l.jpg

PARATHORMONE

  • Secreted into the bloodstream by the parathyroid glands

  • Essential part of the Ca++ homeostatic mechanisms


Parathormone action l.jpg

PARATHORMONE ACTION

  • PTH

    • 1) Increases calcium ion absorption from the intestine

      • Enhances the synthesis of the active form of vitamin D

    • 2) Favors reabsorption of calcium


Parathormone action86 l.jpg

PARATHORMONE ACTION

  • PTH

    • 3) Favors excretion of phosphate (PO4-3) by kidney tubules

    • 4) Enhances bonereabsorption withthe release of Ca++


Parathormone secretion l.jpg

PARATHORMONE SECRETION

  • PTH secretion is:

    • Stimulated by decreased serum level of Ca++

    • Inhibited by increased serum levels of Ca++

Ca++

PTH

Ca++

PTH


Calcitonin l.jpg

CALCITONIN

  • Calcitonin is a hormone secreted by the thyroid gland

  • Effects of calcitonin are weak compared to PTH


Calcitonin89 l.jpg

CALCITONIN

  • Decreases serum Ca++ level by:

    • 1) Interfering with bone resorption

    • 2) Favoring bone uptake of calcium

    • 3) Promoting excretion of calcium by the kidney

CALCITONIN

Calcitonin stimulates calcium salt deposit in bone

Thyroid gland releases calcitonin

Falling blood Ca++ levels

Rising blood Ca++ levels

Osteoclasts degrade bone and release Ca++

PTH

Parathyroid glands release PTH


Stores of calcium l.jpg

STORES OF CALCIUM

bone calcium

renal excretion

extracellular

calcium

intracellular

calcium

absorption from

intestine

  • 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


Hypercalcemia l.jpg

HYPERCALCEMIA

  • A serum calcium level of 10.5 mg / dl or above results in hypercalcemia

Ca++

=

10.5

Hypercalcemia

Ca++

=

9.0

Hypocalcemia


Hypercalcemia92 l.jpg

HYPERCALCEMIA

  • High levels of Ca++:

    • Interfere with nerve impulse

    • Interfere with muscle contraction

    • May cause kidney stones

    • May precipitate out of body tissues (at high levels)


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CAUSES FOR HYPERCALCEMIA

  • 1) Overactive parathyroid glands

  • 2) Hyperthyroidism increases bone resorption

  • 3) Large doses of vitamin D


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CAUSES FOR HYPERCALCEMIA

  • 4) Confinement to bed for weeks at a time

    • Bone reabsorption occurs at a more rapid rate than bone formation

  • 5) Some malignancies secrete hormones that cause bone resorption


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CAUSES FOR HYPERCALCEMIA

  • 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


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MILK-ALKALI SYNDROME

  • Alkalosis promotes hypercalcemia

    • 1) Causes increased kidney resorption of calcium

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


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CAUSES OF HYPERCALCEMIA


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TREATMENT

  • Intravenous or oral administration of phosphate decreases plasma calcium levels by interfering with bone resorption

  • Calcitonin reduces activities of bone destroying cells (osteoclasts)

  • Glucocorticoids inhibit intestinal absorption of calcium


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TREATMENT

  • Some diuretics promote excretion of calcium by the kidneys

  • Infusion of saline (NaCl) or sodiumsulfate (Na2SO4) increases urinary calcium excretion


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HYPOCALCEMIA

  • Defined as a lowserum calcium level

    • Less than 9 mg / dl

Ca++

=

9.0

Hypocalcemia

Ca++

=

10.5

Hypercalcemia


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HYPOCALCEMIA

  • Physiological response to low calcium serum levels

    • Increased secretion of PTH

      • Which increases calcium by favoring bone resorption

        • Intestinal absorption

        • Renal reabsorption


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CAUSES FOR HYPOCALCEMIA

  • 1) Inadequate vitamin D

    • a) Nutritional deficiencies

    • b) Impaired intestinal absorption

      • ex: partial gastrectomy

    • c) Liver or kidney dysfunctioninterferes with formation of active form of vitamin D


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CAUSES FOR HYPOCALCEMIA

  • d) Inadequate exposure to sunlight

    • Reduction in formation of active vitamin D in the skin

  • e) Intestinal or bone unresponsiveness to action ofvitamin D


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CAUSES FOR HYPOCALCEMIA

  • 2) Loss of parathyroid glands or loss of function

  • 3) Pancreatitis

    • Defect in PTH secretion

    • Calcium deposits form in soft tissues


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CAUSES FOR HYPOCALCEMIA

  • 4) Renal failure

    • Reduction in the formation of an active vitamin D metabolite

    • Altered bone response to PTH is also a factor


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CAUSES OF HYPOCALCEMIA


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TREATMENT

  • Calcium salts administered intravenously or orally

    • Calcium gluconate or calcium chloride solutions

  • Vitamin D may be given


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END OFFLUID AND ELECTROLYTES PART 2


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