FLUID AND ELECTROLYTE REGULATION AND ACID BASE BALANCE

1
FLUID AND ELECTROLYTE REGULATION AND ACID BASE
BALANCE
2
EXTRACELLULAR VS INTRACELLULAR FLUIDS
3
EXTRACELLULAR FLUIDS

• INTERSTITIAL OR TISSUE FLUID
• PLASMA
• LYMPH
• CEREBROSPINAL FLUID
• INTRAOCULAR FLUID
• SYNOVIAL FLUID
• PERICARDIAL FLUID
• PLEURAL FLUID
• PERITONEAL FLUID

4
EXTRACELLULAR FLUID COMPOSITION

• PLASMA AND TISSUE FLUIDS VERY SIMILAR
• SEPARATED BY CAPILLARY WALLS THAT ALLOW FAIRLY
  FREE EXCHANGE OF LOW MOLECULAR WEIGHT SUBSTANCES

5
DIFFERENCES

• DUE TO FACT PROTEINS CANNOT PASS THROUGH
  MEMBRANES\
• PROTEINS NORMALLY ANIONS
• LEADS TO MORE SODIUM AND LESS CHLORIDE IN PLASMA
  THAN INTERSTITIAL FLUID

6
COMPOSITION OF INTRACELLULAR FLUID

• SEPARATED FROM EXTRACELLULAR BY CELL MEMBRANE
  THAT IS RELATIVELY IMPERMEABLE TO PROTEINS
• SODIUM POTASSIUM PUMP ACCUMULATES SODIUM TO
  OUTSIDE AND POTASSIUM TO INSIDE

7
REGULATION OF THE INTERNAL ENVIRONMENT

• WATER
• ELECTROLYTES
• KIDNEYS PLAY A MAJOR ROLE

8
SODIUM REGULATION

• MAJOR EXTRACELLULAR CATION
• MAJOR OSMOTIC EFFECTS
• WHERE SODIUM GOES WATER FOLLOWS
• GREATLY AFFECTS PLASMA VOLUME AND BLOOD PRESSURE

9
INGESTION OF SODIUM

• REGULATORY COMPONENT
• HEDONISTIC COMPONENT
• AVERAGE CONSUMPTION IN US IS 10-15 GRAMS PER DAY
• 0.5 GRAMS ARE NEEDED

10
RENAL EXCRETION REABSORPTION OF SODIUM

• KIDNEYS CONTROL BODYS SODIUM LEVELS
• RELATIONSHIP BETWEEN GLOMERULAR FILTRATION RATE
  OF SODIUM AND THE TUBULAR REABSORPTION RATE
  DETERMINES SODIUM EXCRETION
• SODIUM IS FREELY FILTERED

11
FACTORS THAT AFFECT GLOMERULAR FILTRATION RATE

• ARTERIAL BLOOD PRESSURE
• ACTIVITY OF SYMPATHETIC NERVES

12
CONTROL OF SODIUM REABSORPTION

• IMPORTANT IN LONG TERM CONTROL OF SODIUM
  EXCRETION
• ALDOSTERONE
• RENIN-ANGIOTENSIN

13
ALDOSTERONE

• STIMULATES SODIUM REABSORPTION
• DISTAL CONVOLUTED TUBULES
• COLLECTING TUBULES

14
HIGH ALDOSTERONE LEVELS

• ALMOST ALL SODIUM IS REABSORBED
• 0.1 GRAM OF SODIUM EXCRETED

15
LOW ALDOSTERONE LEVELS

• AS MUCH AS 30-40 G OF SODIUM CAN BE EXCRETED

16
REGULATION OF ALDOSTERONE SECRETION

• RENIN
• PRODUCED BY JUXTAGLOMERULAR COMPLEX

17
FACTORS THAT LEAD TO RENIN SECRETION

• DECREASE IN RENAL ARTERIAL PRESSURE
• INCREASE IN ACTIVITY OF SYMPATHETIC NERVES

18
EFFECTS OF RENIN

• CONVERTS ANGIOTENSINOGEN INTO ANGIOTENSIN I

19
FATE OF ANGIOTENSIN I

• PASSES THROUGH LUNGS AND IS CONVERTED INTO
  ANGIOTENSIN II

20
EFFECT OF ANGIOTENSIN II

• STIMULATES ALDOSTERONE RELEASE FROM ADRENAL GLAND

21
EFFECT OF ALDOSTERONE

• STIMULATES REABSORPTION OF SODIUM FORM DISTAL
  CONVOUTED TUBULES AND COLLECTNG TUBULES

22
FACTORS THAT LEAD TO SODIUM EXCRETION

• INCREASE IN SYSTEMIC BLOOD PRESSURE
• INCREASED NERVE IMPULSES FROM CIRCULATORY
  PRESSURE RECEPTORS--THIS CAUSES DECREASED
  ACTIVITY OF SYMPATHETIC NERVES WHICH CAUSES
  DILATION OF AFFERENT ARTERIOLES
• DECREASED RELEASE OF RENIN--DECREASED RELEASE OF
  ALDOSTERONE
• RELEASE OF ATRIAL NATRIURETIC FACTOR

23
NET EFFECT

• INCREASE AMOUNT OF SODIUM IN GLOMERULAR FILTRATE
• DECREASE AMOUNT OF SODIUM REABSORBED FROM TUBULES
• INCREASED EXCRETION OF SODIUM
• BODY LEVELS OF SODIUM DECLINE
• WATER FOLLOWS

24
SODIUM CONCENTRATION VS TOTAL SODIUM CONTENT
25
REGULATION OF WATER CONTENT

• INGESTION
• THIRST
• RENAL EXCRETION

26
INGESTION

• HABIT AND SOCIAL FACTORS USUALLY MORE INFLUENTIAL

27
THIRST

• RESULTS FROM INCREASED OSMOTIC CONCENTATION
• REDUCED PLASMA VOLUME
• OSMORECEPTORS IN HYPOTHALAMUS MONITOR
• MAYBE CIRCULATORY RECEPTORS
• ANGIOTENSIN II

28
EXCRETION OF WATER

• RELATIONSHIP BETWEEN GLOMERULAR FILTRATION RATE
  AND TUBULAR REABSORPTION RATE
• WATER IS FREELY FILTERED FROM PLASMA
• FACTORS THAT AFFECT GLOMERULAR FILTRATION RATE
  AFFECTS WATER EXCRETION
• SODIUM REGULATION ALSO VERY IMPORTANT
• DEPENDENT ON ANTIDIURETIC HORMONE

29
ANTIDIURETIC HORMONE AND WATER EXCRETION

• AFFECTS PERMEABILITY OF COLLECTING TUBULES TO
  WATER
• OSMORECEPTORS IN HYPOTHALAMUS
• CIRCULATORY PRESSURE RECPTORS LEFT ATRIUM OF
  HEART

30
FACTORS THAT INFLUENCE WATER EXCETION

• OSMOTIC PRESSURE OF EXTRACELLULAR FLUID
• RARELY SEPARATE FROM FACTORS THAT INFLUENCE
  SODIUM EXCRETION

31
POTASSIUM REGULATION

• EXTRACELLULAR LEVELS CLOSELY REGULATED
• EXCRETION USUALLY EQUALS THE AMOUNT OF INGESTION
• FREELY FILTERED INTO FILTRATE
• CAN BE SECRETED OR REABSORBED BY TUBULES
• USUALLY ALL IS REABSORBED
• AMOUNT EXCRETED DEPENDS ON HOW MUCH IS SECRETED

32
ROLE OF TUBULAR CELLS IN POTASSIUM EXCRETION

• HIGH CONCENTRATION IN CELLS -- MORE POTASSIUM
  SECRETED
• LOWER CONCENTRATION IN CELLS -- LESS POTASSIUM
  SECRETED

33
ROLE OF ALDOSTERONE IN POTASSIUM EXCRETION

• PROMOTES REABSORPTION OF SODIUM BY TUBULES
• INCREASED POTASSIUM CONCENTRATION IN
  EXTRACELLULAR CELLS BATHING ADRENAL CELLS
  INCREASES ALDOSTERONE SECRETION

34
REGULATION OF CALCIUM

• BONE (CONTAINS 99 OF CALCIUM)
• KIDNEYS
• GI TRACT

35
EFFECTS OF PARATHYROID HORMONE

• INCREASES PLASMA CALCIUM LEVELS
• DECREASES PLASMA PHOSPHATE CONCENTRATIONS
• INCREASES MOVEMENT OF CALCIUM AND PHOSPHATE FROM
  BONE TO EXTRACELLULAR FLUID

36
OSTEOCLASTS

• BREAK DOWN BONE

37
EFFECTS OF PARATHYROID HORMONE ON KIDNEY

• DECREASES THE URINARY EXCRETION OF CALCIUM
• INCREASES EXCRETION OF PHOSPHATE
• ENHANCES TRANSFORMATION OF VITAMIN D3 TO 1,25
  DIHYDROXYCHOLECALCIFEROL

38
1,25 DIHYDROXYCHOLECALCIFEROL

• STIMULATES CALCIUM ABSORPTION BY INTESTINES

39
CONTOL OF PARATHYROID HORMONE SECRETION

• CALCIUM LEVELS THAT BATH CELLS OF PARATHYROID

40
CALCITONIN AND CALCIUM LEVELS

• FROM THYROID GLAND
• LOWERS PLASMA LEVELS OF CALCIUM
• INHIBITS REMOVAL OF CALCIUM FROM BONE INHIBITS
  OSTEOCLASTS
• LESS IMPORTANT THAN PARATHYROID

41
CONTROL OF CALCITONIN SECRETION

• CALCIUM LEVELS THAT BATH CELLS OF THYROID

42
REGULATION OF MAGNESIUM
43
HYPOMAGNESMIA

• RARE DISORDER
• CAUSES
• MALNUTRITION
• ALCOHOLISM
• REDUCED ABSORPTION
• RENAL TUBULE PROBLEMS
• SOME TYPES OF DIURETICS

• INCREASED NEUROMUSCULAR ACTIVITY
• IRRITIBILITY
• INCREASED REFLEXES
• MUSCLE WEAKNESS
• TETANY
• CONVULSIONS

44
HYPERMAGNESMIA

• RARE DISORDER
• CAUSES
• RENAL FAILURE
• ANTACIDS CONTAINING MAGNESIUM

• DEPRESSED SKELETAL MUSCLE CONTRACTIONS
• DEPRESSED OF NERVE FUNCTION
• NAUSEA
• VOMITING
• MUSCLE WEAKNESS
• HYPOTENSION
• BRADYCARDIA
• REDUCTION IN RESPIRATION

45
REGULATION OF PHOSPHATE
46
HYPERPHOSPHATEMIA

• CAUSES
• RENAL FAILURE
• SIDE EFFECTS OF CHEMOTHERAPY
• HYPERPARATHYOIDISM

• REDUCED PLASMA CALCIUM CONCENTRATION
• DUE TO CALCIUM PHOSPHATE DEPOSITED IN TISSUES
• LUNGS
• KIDNEYS
• JOINTS

47
HYPOPHOSPHATEMIA

• CAUSES
• REDUCED ABSORPTION OF MAGNESIUM
• HYPERPARATHYROIDISM
• INCREASED RENAL EXCRETION OF PHOSPHATE

• SYMPTOMS
• REDUCED METABOLIC RATE
• REDUCED OXYGEN TRANSPORT
• WHITE BLOOD CELL FUNCTION REDUCED
• REDUCED BLOOD CLOTTING

48
ACID BASE REGULATION

• ACIDS
• BASES
• p H OF BLOOD
• p H OF INTERSTITIAL FLUIDS
• BUFFER SYSTEMS
• ROLE OF RESPIRATORY SYSTEM
• ROLE OF KIDNEYS

49
ACIDS

• INCREASE HYDROGEN ION CONCENTRATION
• PROTON DONORS

50
BASES

• HYROGEN ACCEPTOR
• PROTON ACCEPTOR

51
STRONG ACIDS

• STRONG--ALMOST TOTALLY DISSOCIATE
• PROVIDE LARGE NUMBERS OF HYDROGEN IONS
• HYDROCHLORIC ACID

52
WEAK ACIDS

• POORLY DISSOCIATE
• DO NOT PROVIDE MANY HYDROGEN IONS
• CARBONIC ACID

53
PHs OF BODY

• RANGE FROM 7.35 TO 7.45
• ARTERIAL BLOOD 7.4
• VENOUS BLOOD 7.35
• INTERSITIAL FLUIDS 7.35

54
EFFECTS OF METABOLISM ON PH

• GENERALLY PRODUCE ACIDIC PRODUCTS
• PHOSPHOROUS AND SULFUR IN PROTEINS
• FATTY ACIDS AND LACTIC ACIDS

55
MECHANISMS TO MAINTAIN PH

• BUFFER SYSTEMS
• RESPIRATORY SYSTEM
• KIDNEYS

56
BUFFER SYSTEMS

• PREVENT EXTREME CHANGES IN p H WHEN ACIDS OR
  BASES ARE ADDED
• CARBONIC ACID-SODIUM BICARBONATE BUFFER SYSTEM
• PLASMA PROTEINS
• INTRACELLULAR PHOSPHATE COMPLEXES
• HEMOGLOBIN

57
CARBONIC ACID-SODIUM BICARBONATE BUFFER SYSTEM
58
CARBONIC ACID

• WEAK ACID
• PARTIALLY DISSOCIATE TO FORM HYDROGEN IONS (H)
  BICARBONATE IONS (HCO3-)
• MIXTURE OF DISSOCIATED ACID AND UNDISSOCIATED
  ACID

59
SODIUM BICARBONATE

• DISSOCIATES TO SODIUM IONS (H) BICARBONATE
  IONS (HCO3-)

60
FUNCTION OF BUFFER SYSTEM

• HYDROGEN IONS ARE PICKED UP BY BICARBONATE TO
  FORM CARBONIC ACID
• HYDROXIDE IONS ARE PICKED UP BY HYDROGEN IONS TO
  MAKE WATER
• CARBONIC ACID DISSOCIATES TO REPLACE HYDROGEN
  IONS
• STABILIZES p H

61
BUFFERS ALONE CAN NOT MAINTAIN NORMAL p H
62
REGULATION OF ACID BASE BALANCE BY THE
RESPIRATORY SYSTEM

• CARBONIC ACID IN BLOOD IS IN EQUILIBRIUM WITH
  CARBON DIOXIDE AND WATER
• ELIMINATION OF LARGE AMOUNTS OF CARBON DIOXIDE
  AT LUNGS REDUCES ACIDITY
• REDUCED ELIMINATION OF CARBON DIOXIDE AT LUNGS
  INCREASES ACIDITY

63
REGULATION OF ACID BASE BALANCE BY THE URINARY
SYSTEM

• HYDROGEN IONS SECRETED INTO TUBULES
• BICARBONATE IONS IN FILTRATE REABSORBED BY
  TUBULAR CELLS
• PHOSPHATE COMPOUNDS
• AMMONIA

64
SECRETION OF HYDROGEN IONS

• SECRETED BY TUBULAR CELLS
• HYDROGEN IONS DERIVED FROM CARBONIC ACID
• CARBONIC ANHYDRASE CATALYZES REACTION TO FORM
  CARBONIC ACID
• HYDROGEN IONS TO TUBULES -- BICARBONATE TO BLOOD

65
REABSORPTION OF BICARBONATE IONS

• SECRETION OF HYDROGEN ALLOWS RECOVERY OF
  BICARBONATE IONS FROM FILTRATE
• HYDROGEN IONS COMBINE WITH BICARBONATE TO FORM
  CARBONIC ACID
• DISSOCIATE INTO CARBON DIOXIDE AND WATER
• MEMBRANE ASSOCIATED CARBONIC ACID CATALYZES
  REACTION
• CARBON DIOXIDE ENTERS CELLS
• CARBONIC ACID IS FORMED
• DISSOCIATES AND HYDROGEN IONS ENTER THE
  LUMEN--BICARBONATE ENTERS THE BLOOD

66
FACTORS CONTROLLING HYDROGEN ION SECRETION AND
BICARBONATE ION REABSORPTION

• DEPENDENT ON PRESENCE OF HYDROGEN IONS IN TUBULES
• VARIES WITH ACIDITY OF BODY
• USUALLY SLIGHTLY MORE HYDROGEN IONS ARE SECRETED
  THAN BICARBONATE IONS REABSORBED

67
FALLING CONCENTRATIONS OF HYDROGEN IONS IN BODY

• RATE OF HYDROGEN SECRETION REDUCES RELATIVE TO
  BICARBONATE ION FILTRATOIN RATE
• NOT ALL BICARBONATE IS REABSORBED AND IS EXCRETED
  IN URINE
• DIMINISHES BICARBONATE IN BODY RAISES HYDROGEN
  ION CONCENTRATION TOWARDS NORMAL

68
INCREASING CONCENTRATIONS OF HYDROGEN IONS IN BODY

• RATE OF HYDROGEN SECRETION INCREASED RELATIVE TO
  BICARBONATE ION FILTRATION RATE
• EXCESS OF HYDROGEN IONS
• EXCESS EXCRETED IN URINE
• INCREASED BICARBONATE IONS IN BODY TIES UP
  HYDROGEN IONS AND WITH OTHER BUFFER SYSTEMS
  DECREASE HYDROGEN ION CONCENTRATIONS

69
BUFFERING OF SECRETED HYDROGEN IONS

• SECRETION OF HYDROGEN IONS COULD REDUCE p H TO
  AS LOW AS 4.5
• THIS CONCENTRATION IS NOT SUFFICIENT TO GET RID
  SUFFICIENT NUMBERS OF HYDROGEN IONS
• BUFFERS ALLOW US TO KEEP p H ABOVE 4.5 AND STILL
  ELIMINATE SUFFICIENT HYDROGEN IONS

70
PHOSPHATE BUFFERS

• HPO4-
• TIES UP HYDROGEN IONS IN TUBULAR FLUID
• FOUND IN FILTRATE
• POORLY REABSORBED
• COMBINE WITH HYDROGEN IONS
• SECRETED WITH SODIUM AS WEAK ACID

71
AMMONIA BUFFERS

• FORMED BY TUBULAR CELLS
• DEAMINATION OF GLUTAMIC AND OTHER AMINO ACIDS
• DIFFUSES INTO LUMEN FROM TUBULAR CELL
• COMBINES WITH HYDROGEN IONS TO FORM AMMONIUM IONS
• REMOVES BOTH HYDROGEN AND AMMONIA IONS FROM
  TUBULAR FLUID
• THIS ALLOWS MORE AMMONIA TO DIFFUSE INTO TUBULES
• EXCRETED IN COMBINATION WITH CHLORIDE AND OTHER
  ANIONS

72
ACIDOSIS VS ALKALOSIS

• 7.35-7.45

73
ACIDOSIS

• ABNORMAL INCREASE OF HYDROGEN IONS IN BLOOD
• RESPIRATORY ACIDOSIS
• METABOLIC ACIDOSIS

74
RESPIRATORY ACIDOSIS

• DUE TO INCREASE IN CARBON DIOXIDE AND CARBONIC
  ACID CONCENTRATIONS
• CAUSED BY ASPHYXIA OR DISESES THAT INTERFERE WITH
  ELIMINATION OF CARBON DIOXIDE BY LUNGS

75
METABOLIC ACIDOSIS

• CAUSED BY ANY OTHER INCREASE IN HYDROGEN IONS
• SEVERE DIARRHEA
• VOMITING
• KETOSIS
• INGESTION OF ACIDIC DRUGS

76
ALKALOSIS

• ABNORMAL DECREASE IN HYDROGEN ION CONCENTRATION
  IN BLOOD
• RESPIRATORY ALKALOSIS
• METABOLIC ALKALOSIS

77
RESPIRATORY ALKALOSIS

• DECREASE IN CARBON DIOXIDE AND CARBONIC ACID
  CONCENTRATIONS
• OVERVENTILATION
• NOT COMMON

78
METABOLIC ALKALOSIS

• CAUSED BY ANY OTHER FACTOR
• VOMITING OF GASTRIC CONTENTS ONLY
• ALKALINE DRUGS

79
ACIDEMIA

• p H OF ARTERIAL BLOOD FALLS BELOW 7.35
• DEPRESSES NERVOUS SYSTEM
• COMA

80
ALKALEMIA

• p H OF ARTERIAL BLOOD RISES ABOVE 7.45
• USUALLY CANNOT LIVE MORE THAN A FEW HOURS IF
  RISES ABOUT 8.0
• OVEREXCITABILITY OF NERVOUS SYSTEM
• TETANY OF MUSCLES
• EXTREME NERVOUSNESS
• CONVULSIONS IN SOME