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1 ADVANCED PHYSIOLOGY FLUID & ELECTROLYTES PART 2 Instructor Terry Wiseth NORTHLAND COLLEGE.

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Presentation on theme: "1 ADVANCED PHYSIOLOGY FLUID & ELECTROLYTES PART 2 Instructor Terry Wiseth NORTHLAND COLLEGE."— Presentation transcript:

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2 1 ADVANCED PHYSIOLOGY FLUID & ELECTROLYTES PART 2 Instructor Terry Wiseth NORTHLAND COLLEGE

3 2 ELECTROLYTE BALANCE The exchange of interstitial and intracellular fluid is controlled mainly by the presence of the electrolytes sodium and potassium Na + K+K+K+K+ K+K+K+K+ K+K+K+K+ K+K+K+K+

4 3 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+

5 4 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 K+K+K+K+ H2OH2O H2OH2O H2OH2O H2OH2O H2OH2O H2OH2O H2OH2O H2OH2O K+K+K+K+ K+K+K+K+ K+K+K+K+ Na + Click to see animation

6 5 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 K+K+K+K+ H2OH2O H2OH2O H2OH2O H2OH2O H2OH2O H2OH2O H2OH2O H2OH2O K+K+K+K+ K+K+K+K+ K+K+K+K+ Na + Click to see animation

7 6 ELECTROLYTE BALANCE Aldosterone, ANP and ADH regulate sodium levels within the body, while aldosterone can be said to regulate potassium K+K+K+K+ Na + aldosterone ADH ANP

8 7 ELECTROLYTE BALANCE Na + Sodium (Na + ) ions are the important cations in extracellular fluid Cl - HCO 3 - Anions which accompany sodium are chloride (Cl - ) and bicarbonate (HCO 3 - ) Considered an indicator of total solute concentration of plasma osmolality Na + HCO 3 - Cl -

9 8 H2OH2O H2OH2O H2OH2O H2OH2O H2OH2O H2OH2O ELECTROLYTE BALANCE Sodium Sodium ions are osmotically important in determining water movements A discussion of sodium must also include  Chlorine  Bicarbonate  Hydrogen ions Potassiumcalcium Potassium and calcium serum concentrations are also important electrolytes in the living system H2OH2O H2OH2O H2OH2O H2OH2O H2OH2O H2OH2O H2OH2O H2OH2O H2OH2O

10 9 Click Hypercalcemia Hypercalcemia - elevated calcium levels Hypokalcemia Hypokalcemia -- lowered calcium levels Click Hyperkalemia Hyperkalemia -- elevated potassium levels Hypokalemia Hypokalemia ---- lowered potassium levels Hypernatremia Hypernatremia - elevated sodium levels Hyponatremia Hyponatremia -- lowered sodium levels ELECTROLYTE BALANCES

11 10 HYPERNATREMIA Normal range for blood levels of sodium is app meq/liter Hypernatremia Hypernatremia refers to an elevated serum sodium level ( meq/liter) Increased levels of sodium ions are the result of diffusion and osmosis Na +

12 SODIUM PRINCIPLES 1) Sodium ions do not cross cell membranes as quickly as water does Na + H2OH2O H2OH2O H2OH2O H2OH2O H2OH2O

13 12 SODIUM PRINCIPLES 2) Cells pump sodium ions out of the cell by using sodium-potassium pumps Na +

14 13 SODIUM PRINCIPLES 3) Increases in extracellular sodium ion levels do not change intracellular sodium ion concentration Na +

15 14 RESULTS OF HYPERNATREMIA 1) Water is osmotically drawn out of the cells  Resulting in dehydration 2) Increase in extracellular fluid volume Extracellular fluid volume Intracellular fluid volume

16 15 CNS REACTION TO HYPERNATREMIA In the CNS tight junctions exist between endothelial cells of the capillary walls 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 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 Increased levels of sodium ions in the blood does not result in increased sodium ions in brain interstitial fluid

17 16 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 H2OH2O

18 17 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

19 18 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 H2OH2O

20 19 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

21 20 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)

22 21 Glucose 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 Glucose H2OH2O H2OH2O H2OH2O H2OH2O H2OH2O H2OH2O H2OH2O H2OH2O H2OH2O H2OH2O H2OH2O H2OH2O Click to animate

23 22 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

24 23 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

25 24 CAUSES OF HYPERNATREMIA

26 25 TREATMENT OF HYPERNATREMIA Re-hydration is the primary objective in most cases  Decreases sodium concentrations A point of concern is when and how rapid the re-hydration occurs

27 26 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 cerebral edema with fluid being drawn into brain tissues

28 27 TREATMENT OF HYPERNATREMIA Treatment is best handled by giving slow infusions of glucose solutions  This dilutes high plasma sodium ion concentrations

29 28 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

30 29 Defined as a serum sodium ion level that is lower than normal Implies an increased ratio of water to sodium in extracellular fluid  Extracellular fluid is more dilute than intracellular fluid  Results in a shift of water into cells HYPONATREMIA

31 30 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

32 31 GENERAL RESPONSE TO HYPONATREMIA Suppression of thirst Suppression of ADH secretion  Both favor decreasing water ingestion and increasing urinary output

33 32 SYMPTOMS OF HYPONATREMIA Primarily neurological (net flux of water into the brain) 125 meq / liter Sodium ion levels of 125 meq / liter are enough to begin the onset of symptoms 110meq / liter Sodium ion levels of less than 110 meq / liter bring on seizures and coma

34 33 HYPONATREMIA Produced by:  1) A loss of sodium ions  2) Water excess  Water excess can be due to:  Ingestion  Renal retention

35 34 DILUTIONAL EFFECT 1) Isotonic fluid loss 1) Isotonic fluid loss 2) Antidiuretic hormone secretion 2) Antidiuretic hormone secretion 3) Acute or chronic renal failure 3) Acute or chronic renal failure 4) Potassium ion loss 4) Potassium ion loss 5) Diuretic therapy 5) Diuretic therapy H2OH2O H2OH2O H2OH2O H2OH2O H2OH2O H2OH2O Na + H2OH2O H2OH2O H2OH2O H2OH2O H2OH2O H2OH2O H2OH2O H2OH2O H2OH2O H2OH2O H2OH2O H2OH2O H2OH2O

36 35 DILUTIONAL EFFECT 1) Isotonic fluid loss 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

37 36 DILUTIONAL EFFECT 2) Antidiuretic hormone secretion 2) Antidiuretic hormone secretion  Enhances water retention 3) Acute or chronic renal failure 3) Acute or chronic renal failure  The kidney fails to excrete water  Can lead to hyponatremia

38 37 DILUTIONAL EFFECT 4) Potassium ion loss 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

39 38 POTASSIUM ION LOSS K+K+K+K+ Na + K+K+K+K+ K+K+K+K+ K+K+K+K+ 1) extracellular potassium loss potassium loss 2) diffusion of potassium ions into extracellular compartments 3) intracellular electrical balance is maintained by diffusion of sodium ions into cells plasma interstitial fluid cell

40 39 POTASSIUM ION LOSS K+K+K+K+ Na + K+K+K+K+ K+K+K+K+ K+K+K+K+ Plasma Interstitial fluid Cell K+K+K+K+ K+K+K+K+ Na + Click to see animation

41 40 DILUTIONAL EFFECT DILUTIONAL EFFECT 5) Diuretic therapy 5) Diuretic therapy  Common cause of hyponatremia  Loss of sodium and potassium often occurs in addition to fluid loss

42 41 CAUSES OF HYPONATREMIA

43 42 REACTIONS TO HYPONATREMIA Increased Na + Osmoreceptors inhibited Decreased ADH release Decreased Thirst Increased urinary H 2 O loss Decreased H 2 O gain Decreased Na + Homeostasis Normal Na + Osmoreceptors stimulated Increased ADH release Increased Thirst Additional H 2 O dilutes Na + H 2 O loss concentrates Na + Decreased urinary H 2 O loss Increased H 2 O gain Click to view increased Na + Click to view decreased Na +

44 43 HYPERKALEMIA Normal serum potassium level (3-5 meq / liter) Normal serum potassium level (3-5 meq / liter)  As compared to Na + (142 meq / liter) Intracellular levels of potassium ( meq / liter) Intracellular levels of potassium ( meq / liter)  This high intracellular level is maintained by active transport by the sodium-potassium pump K+K+

45 44 Na + / K + Pump Cells pump K + ions in and Na + ions out of the cell by using sodium-potassium pumps Na + K+K+ K+K+ K+K+ K+K+

46 45 HYPERKALEMIA Hyperkalemia K + Hyperkalemia is an elevated serum potassium (K + ) ion level acidosis A consequence of hyperkalemia is acidosis H +  an increase in H + ions in body fluids K + H + Changes in either K + or H + ion levels causes a compartmental shift of the other K+K+

47 46 HYPERKALEMIA When hyperkalemia develops potassium ions diffuse into the cell 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 As a result the physiological response to hyperkalemia causes acidosis K+K+ K+K+ K+K+ K+K+ K+K+ K+K+ H+H+ H+H+ H+H+ H+H+ H+H+ H+H+ H+H+ H+H+ H+H+ HYPERKALEMIA

48 47 HYPERKALEMIA The reverse occurs as well The reverse occurs as well The body is protected from harmful effects of an increase in extracellular H + ions (acidosis) 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 This causes a shift of potassium ions out of the cells H+H+ H+H+ H+H+ H+H+ H+H+ H+H+ H+H+ H+H+ H+H+ K+K+ K+K+ K+K+ K+K+ K+K+ K+K+ ACIDOSIS

49 48 HYPERKALEMIA Summarized:  Hyperkalemia causes acidosis  Acidosis causes hyperkalemia HYPERKALEMIA H+H+ H+H+ H+H+ H+H+ H+H+ H+H+ H+H+ H+H+ K+K+ K+K+ K+K+ K+K+ K+K+ K+K+ K+K+ K+K+ ACIDOSIS

50 49 HYPERKALEMIA Summarized:  Hyperkalemia causes acidosis  Acidosis causes hyperkalemia HYPERKALEMIA H+H+ H+H+ H+H+ H+H+ H+H+ H+H+ H+H+ H+H+ K+K+ K+K+ K+K+ K+K+ K+K+ K+K+ K+K+ K+K+ ACIDOSIS

51 50 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

52 51 CAUSES FOR HYPERKALEMIA 1) Increased input of potassium 2) Impaired excretion of potassium 3) Impaired uptake of potassium by cells

53 52 INCREASED INPUT KCl A) Intravenous KCl infusion K + B) Use of K + containing salt substitutes K + C) Hemolysis of RBC during blood transfusions with release of K + K + D) Damaged and dying cells release K +  Burns, crush injuries, ischemia E) Increased fragility of RBC

54 53 CELLULAR-EXTRACELLULAR SHIFTS Insulin deficiency predisposes an individual to hyperkalemia K + insulin, aldosterone and epinephrine Cellular uptake of K + ions is enhanced by insulin, aldosterone and epinephrine K +  Provides protection from extracellular K + overload Insulin K+K+ K+K+ K+K+ K+K+ K+K+ K+K+ Click to view animation

55 54 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 +

56 55 HYPERKALEMIC PERIODIC PARALYSIS K + Inherited disorder in which serum K + level rise periodically K +  Caused by a shift of K + from muscle to blood in response to ingestion of potassium or exercise  Reasons for the shift are not clear Attacks are characterized by muscle weakness

57 56 RENAL INSUFFICIENCY Aldosterone has a primary role in promoting: Na +  Conservation of Na + K +  Secretion of K + by the nephrons of the kidney Addison’s disease is characterized by aldosterone deficiency  Thus the kidney is unable to secrete potassium at a normal rate

58 57 OLIGURIC RENAL FAILURE Kidney loses the ability to secrete K +

59 58 SPINOLACTONE Diuretic that is antagonistic to the effects of aldosterone K + K +  Causes some rise in serum K + levels by interfering with K + secretion in the kidneys Increases may not be significant  But individuals taking the diuretic are at risk if potassium is administered

60 59 TREATMENT K + 1) Counteract effects of K + ions at the level of the cell membrane K + 2) Promotion of K + ion movements into cells K + 3) Removal of K + ions from the body

61 60 SALT INFUSIONS calcium gluconate or NaCl Infusion of calcium gluconate or NaCl solutions K +  Immediately counteract the effects of K + ions on the heart  Effective for only 1-2 hours

62 61 SODIUM BICARBONATE NaHCO 3 NaHCO 3 also reverses hyperkalemic effects on the heart If acidosis is a factor also raises the pH of body fluids

63 62 INSULIN-GLUCOSE INFUSION Insulin given with glucose  Effective in about 30 minutes  Has a duration of action of up to 6 hours K + Insulin promotes the shift of K + ions into cells Glucose prevents insulin- induced hypoglycemia

64 63 KAYEXALATE (cation exchange resin) Kayexalate (cation exchange resin) K + K + Na +  Removes K + ions from the body by exchanging K + for Na +  Exchange time is about 45 minutes  Effective for up to 6 hours

65 64 DIALYSIS Peritoneal dialysis or hemodialysis K + Effectively clears the blood of high K + levels as well

66 65 CAUSES OF HYPERKALEMIA

67 66 HYPOKALEMIA K + (< 3 meq / liter) Defined as a serum K + level that is below normal (< 3 meq / liter) Serum concentrations will decrease if: K +  There is an intracellular flux of K +  K +  K + ions are lost from the gastrointestinal or urinary tract K+K+K+K+

68 67 ALKALOSIS 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 K+K+K+K+ H+H+H+H+ HCO 3 -

69 68 ALKALOSIS H + Alkalosis elicits a compensatory response causing H + ions to shift from cells to extracellular fluids  This corrects the acid-base imbalance HCO 3 - H+H+H+H+ H+H+H+H+ H+H+H+H+ H+H+H+H+ H+H+H+H+ H+H+H+H+ H+H+H+H+ H+H+H+H+

70 69ALKALOSIS K + H + ions are exchanged for K + (potassium moves into cells) K +  Thus serum concentrations of K + are decreased  And alkalosis causes hypokalemia HCO 3 - H+H+H+H+ H+H+H+H+ H+H+H+H+ H+H+H+H+ H+H+H+H+ H+H+H+H+ H+H+H+H+ H+H+H+H+ K+K+K+K+ K+K+K+K+ K+K+K+K+ K+K+K+K+ K+K+K+K+ K+K+K+K+ K+K+K+K+ K+K+K+K+

71 70 ALKALOSIS Conversely when K + ions are lost from the cellular and extracellular compartments  Sodium and hydrogen ions enter cells in a ratio of 2:1 as replacement This loss of extracellular H + causes alkalosis HCO 3 - H+H+H+H+ K+K+K+K+ H+H+H+H+ H+H+H+H+ H+H+H+H+ H+H+H+H+ H+H+H+H+ H+H+H+H+ Na + K+K+K+K+ K+K+K+K+ K+K+K+K+ K+K+K+K+ K+K+K+K+ K+K+K+K+ K+K+K+K+

72 71 KIDNEY FUNCTION Kidney function is altered by hypokalemia  Na + K +  Na + ions are reabsorbed into the blood when K + ions are secreted into the urine by kidney tubules K+K+ Tubular lumen K+K+ K+K+ K+K+ K+K+ K+K+ K+K+ Na + Peritubular fluid NORMAL

73 72 KIDNEY FUNCTION Kidney function is altered by hypokalemia K +  If adequate numbers of K + are not available for this exchange  H +  H + ions are secreted instead H+H+ Tubular lumen K+K+ H+H+ K+K+ H+H+ K+K+ H+H+ Na + Peritubular fluid HYPOKALEMIA

74 73 KIDNEY FUNCTION H + Hypokalemia promotes renal loss of H + ions and thus results in alkalosis

75 74 NORMAL NEPHRON Normal nephron function is to secrete H + and K + in exchange for Na + capillary distal tubule H+H+ K+K+ Na + Blood Urine

76 75 NEPHRON ACTION IN HYPOKELEMIA capillary distal tubule H+H+ K+K+ Na + Hypokalemia In Hypokalemia the kidney selectively secretes H + H + ions in preference K + to K + ions H + The loss of H + ions may lead to alkalosis Blood Urine

77 76 ALKALOSIS capillary distal tubule H+H+ K+K+ Na + retained K+K+ excreted 1) in alkalosis there is a decrease in extracellular H + fluid H + 2) the kidney retains hydrogen ions to correct the alkalosis K + Hypokalemia 3) the kidney then eliminates K + ions which can lead to Hypokalemia Blood Urine

78 77 CAUSES OF HYPOKALEMIA

79 78 TREATMENT OF HYPOKALEMIA Replacement of K + either by: K +  Oral K + salt supplements  Diet K +  Intravenous administration of K + salt solution (spinolactone)  Diuretic (spinolactone) if renal loss is at work

80 79 CALCIUM HOMEOSTASIS Ca ++ Ca ++ plays an important role in:  Muscle contraction  Nerve impulse transmission  Hormone secretion  Blood clotting

81 80 CALCIUM HOMEOSTASIS Normal range for serum calcium is mg/dl ( meq / liter) The range for proper function has narrow limits Ca ++ = 4.9 meq / liter

82 81 VITAMIN D Vitamin D Vitamin D is involved in maintaining serum Ca ++ levels

83 82 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

84 83 VITAMIN D Vitamin D enhances serum Ca ++ levels by:  1)  1) Directly promoting bone resorption with the release of chemical salts  2) parathormone (PTH)  2) Potentiating the effects of parathormone (PTH) on bone reabsorption  3)Ca ++  3) Increasing absorption of Ca ++ ions from the intestine  4)  4) Reabsorption by the kidney tubules

85 84 PARATHORMONE Secreted into the bloodstream by the parathyroid glands Essential part of the Ca ++ homeostatic mechanisms

86 85 PARATHORMONE ACTION PTH  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

87 86 PARATHORMONE ACTION PTH  3)PO 4 -3  3) Favors excretion of phosphate (PO 4 -3 ) by kidney tubules  4) Ca ++  4) Enhances bone reabsorption with the release of Ca ++

88 87 PARATHORMONE SECRETION PTH secretion is:  Stimulated Ca ++  Stimulated by decreased serum level of Ca ++  Inhibited Ca ++  Inhibited by increased serum levels of Ca ++ PTH Ca ++ PTH

89 88 CALCITONIN thyroid gland Calcitonin is a hormone secreted by the thyroid gland Effects of calcitonin are weak compared to PTH

90 89 Rising blood Ca ++ levelsCALCITONIN Decreases 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 ++ PTH CALCITONIN

91 90 STORES OF CALCIUM bone calcium intracellularcalcium extracellularcalcium renal excretion 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

92 91 HYPERCALCEMIA A serum calcium level of 10.5 mg / dl or above results in hypercalcemia Ca ++ Hypercalcemia10.5 = Hypocalcemia9.0 =

93 92 HYPERCALCEMIA High 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)

94 93 CAUSES FOR HYPERCALCEMIA 1) 1) Overactive parathyroid glands 2) 2) Hyperthyroidism increases bone resorption 3) 3) Large doses of vitamin D

95 94 CAUSES FOR HYPERCALCEMIA 4) 4) Confinement to bed for weeks at a time  Bone reabsorption occurs at a more rapid rate than bone formation 5) 5) Some malignancies secrete hormones that cause bone resorption

96 95 CAUSES FOR HYPERCALCEMIA 6) 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

97 96 MILK-ALKALI SYNDROME  Alkalosis promotes hypercalcemia  1)  1) Causes increased kidney resorption of calcium  2)  2) Decreases the capacity of bone to take up additional calcium

98 97 CAUSES OF HYPERCALCEMIA

99 98 TREATMENT phosphate Intravenous or oral administration of phosphate decreases plasma calcium levels by interfering with bone resorption Calcitonin Calcitonin reduces activities of bone destroying cells (osteoclasts) Glucocorticoids Glucocorticoids inhibit intestinal absorption of calcium

100 99 TREATMENT diuretics Some diuretics promote excretion of calcium by the kidneys saline (NaCl) sodiumsulfate (Na 2 SO 4 ) Infusion of saline (NaCl) or sodium sulfate (Na 2 SO 4 ) increases urinary calcium excretion

101 100 HYPOCALCEMIA low Defined as a low serum calcium level  Less than 9 mg / dl Ca ++ Hypercalcemia10.5 = Hypocalcemia9.0 =

102 101 HYPOCALCEMIA Physiological response to low calcium serum levels  Increased secretion of PTH  Which increases calcium by favoring bone resorption  Intestinal absorption  Renal reabsorption

103 102 CAUSES FOR HYPOCALCEMIA 1) Inadequate vitamin D 1) Inadequate vitamin D  a)  a) Nutritional deficiencies  b)  b) Impaired intestinal absorption  ex: partial gastrectomy  c)  c) Liver or kidney dysfunction interferes with formation of active form of vitamin D

104 103 CAUSES FOR HYPOCALCEMIA  d)  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

105 104 CAUSES FOR HYPOCALCEMIA 2) Loss of parathyroid glands or loss of function 2) Loss of parathyroid glands or loss of function 3) Pancreatitis 3) Pancreatitis  Defect in PTH secretion  Calcium deposits form in soft tissues

106 105 CAUSES FOR HYPOCALCEMIA 4) Renal failure 4) Renal failure  Reduction in the formation of an active vitamin D metabolite  Altered bone response to PTH is also a factor

107 106 CAUSES OF HYPOCALCEMIA

108 107 TREATMENT Calcium salts administered intravenously or orally  Calcium gluconate or calcium chloride solutions Vitamin D may be given

109 108 END OF FLUID AND ELECTROLYTES PART 2


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