Sodium And Water

Front 1

Osmolality

Back 1

Concentration of solute per kg of solvent

Front 2

Osmolarity

Back 2

Concentration of solute per liter of solvent

Front 3

Tonicity

Back 3

Concentration of non-penetrating (effective) osmoles of solute per liter

Front 4

Specific gravity

Back 4

weight of substance vs weight of an equal vol of DW

Front 5

Osmotic pressure

Back 5

=nCRT

n= dissociable particles per molecule
C= concentration of solute in solvent
R = 0.82
T = absolute temperature

Front 6

Common isotonic solns

Back 6

NS - 154 meq/L, 308 mosm/L

Ringer's lactate - 130 meq/L, 279 mosm/L

Front 7

D5W

Back 7

5% dextrose in water
278 mosm/L rapidly metabolized to 0 mosm
Hypotonic solution

Front 8

Hypertonic IV solution

Back 8

3% NaCl
513 mEq/L, 1026 msom/L

Front 9

Hypo/hypernatremia are problems of

Back 9

Water

Front 10

Hypo/hypervolemia are problems of

Back 10

Salt

Front 11

Primary osmoles of human body

Back 11

Extra cellular - sodium
Intra cellular - potassium

Front 12

What is total body water %?

Back 12

50-60%

Front 13

How does water move in the body?

Back 13

Freely between the intracellular, intravascular, and interstitital compartments

Changes is osmolarity are rapidly balanced by redistribution of water

Front 14

Body osmolarity

Back 14

Normally 280-290

Estimated by
2[Na] + [glucose]/18 + [BUN]/2.8

(actually will be a little higher 2/2 Ca, PO4, albumin, etc)

Front 15

How is plasma osmolarity measured?

Back 15

Freezing point depression

Front 16

Gap between calculated and measured plasma osmolarity?

Back 16

>10 mosm/L difference indicates that an unmeasured solute is present

ex: alcohol, paraproteins

Front 17

What makes an osmole effective?

Back 17

Sequestration in to one compartment

Front 18

Result from changes in Na concentration

Back 18

Change in body water distribution
Not necessarily a change in total body water

Front 19

Idiogenic osmoles

Back 19

Brain cells make organic solutes to resist changes to osmolarity (volume)

Ex. Inositol, amino acids

2-3 days to replace or remove

Front 20

Osmoregulation

Back 20

Hypothalamic sensors

Increase triggers thirst and ADH

Front 21

ADH actions generally

Back 21

Renal conservation of water

Peripheral vasoconstriciton

Front 22

Renal water handling overview

Back 22

Isotonic glomerular filtration
Water follows solutes passively in PCT
Independent sodium resorption in loop
Independent water resorption in collecting duct

Front 23

What effects how much urine can be produced?

Back 23

Dilution ability of kidney
Total osmolar consumption

Front 24

Collecting duct, what happens?

Back 24

In the absence of ADH, urine dilutes via sodium reabsorption
With ADH, urine concentrates as water is reabsorped when urine passes by hypertonic medulla

Front 25

Limiting factor in ability to concentrate urine

Back 25

Medullary concentration gradient

Maximal osmolality of medulla is 1200 mosm/L

Front 26

Volume regulation

Back 26

JGA senses Na flow rate
drops stimulate the RAA

Baroreceptor in the carotid sinus sense decreases arterial pressure
stimulates adrenergic system, ADH release

Atrial stretch receptors sense vol expansion
stimulate ANP release

Front 27

Effective circulating volume

Back 27

Perfusing, bioavailable blood

Blood moving through arterial circulation and into capillaries

Front 28

What decreases effective circulating volume

Back 28

Hypovolemia
Edematous states increase the interstitial percentage
Venous obstruction or pooling can trap

Front 29

What increases ECV

Back 29

Volume overload

Maintained by kidney failure or abnormal fluid retention (hyperaldosteronemia)

Front 30

Manifestations of increased ECV

Back 30

HTN

Front 31

Is this edematous state increased ECV or decreased ECV?

Back 31

Are tissues being appropriately perfused?

Front 32

Body's response to decreased ECV

Back 32

Increased CO (HR and inotropy)

Increased peripheral vascular resistance

Increase intravascular vol from (Na/ water)

Front 33

JGA stimuli

Back 33

Renal hypoperfusion
sensed by reduced Na passage
also beta one

Front 34

Angiotensin II

Back 34

Direct vasoconstricter
particularly of efferent arteriole
Increased Na and HCO3 reabsorption in PCT

Stimulates aldosterone release

Front 35

Aldosterone

Back 35

Made in adrenal cortex

Acts in collecting duct

Stimulates Na channels in principal cells
Enhances Na absorption, K secretion

Stimulates H secretion in intercalated cells

Front 36

ANP

Back 36

Atrial naturetic peptide

Direct vasodilator
Lower BP
Afferent arteriole dilation leads to increased GFR

Stimulates Na excretion

Front 37

Response to increased ECV

Back 37

Elevated BP triggers Na diuresis in normal subjects
Increased renal blood flow
Suppression of renin
ANP

Front 38

Hyper and hyponatremia are disorders of...

Back 38

Water regulation

Front 39

Hypernatremia

Back 39

Too little water for the amount of salt presetn

Front 40

Causes of hypernatremia

Back 40

Water loss -- almost always
rare if pts have free access to water

Rare iatrogenic from hypertonic saline, NaHCO3 treatment
Rare halophagia

Front 41

What determines symptoms associated with electrolyte disturbances

Back 41

Rate of onset

Idiogenic osmoles mitigate osmolar changes that are >24-48 hours

Front 42

Symptoms of hypernatremia

Back 42

Lethargy or irritability
Weakness
Seizures
Coma

Front 43

Where is water lost by body?

Back 43

Renal
GI
Insensible losses

Front 44

Diabetes insipidus types

Back 44

Central - problem with hypothalmic destruction
Nephrogenic - lack of response to ADH by kidney (ex Lithium)
Peripheral ADH destruction -- vasopressinase related to pregnancy

Front 45

When do kidneys lose an inappropriate amount of water

Back 45

When ADH is absent, ineffective, or overcome by osmotic diuresis

Front 46

Diabetes insipidus

Back 46

Inability to conserve water
Produciton of dilute urine regardless of serum osmolality
3-20 L daily
Polyuria without regard to vol/osmolar status

Hypernatremia results when polydipsia does not

Front 47

Treating central diabetes insipidus

Back 47

Exogenous vasopressin

DDAVP nasal spray

Front 48

Causes of nephrogenic DI

Back 48

Lack of response to ADH

Lithium, dimeclocycline via tubular damage that is irreversible

Hypokalemia, hypercalcemia -- reversible

Front 49

Osmotic causes of excess renal water loss

Back 49

Glucose - diabetes mellitus
Mannitol
Hypertonic saline
Large osmolar load -- high protein diet, parenteral nutrition

Front 50

GI losses of water

Back 50

Diarrhea is usually hypotonic

Vomit is hypotonic and impairs access to water

Front 51

Insensible losses of water

Back 51

Sweat is hypotonic
Evaporative loss is very hypotonic

Fever or skin break increase insensible loss

Normally 400 ccs/m2/d

Front 52

Isothenuria

Back 52

Urine osmoles = plasma osmoles

Osmotic diuresis

Front 53

Urine osmolarity in hypernatremia

Back 53

High urine osmolarity >500 is appropriate

Low urine osmolarity (below serum) is inappropriate in hyper natremia
DI

Front 54

Treatment of hypernatremia

Back 54

Acute (<24 hours) can be corrected rapidly
Chronic hypernatremia requires slow correction (idiogenic osmoles)
rapid correction -- cerebral edema

10-12/meq/day

Front 55

Rate of correction for hypernatremia

Back 55

Desired change in sodium
Multiplied by two = hours to correct

Totally water deficit/ hours to correct = rate

Use NS in volume deplete patients, half in euvolemic

Plus ongoing losses

Front 56

Hyponatremia

Back 56

Low serum sodium

Usually hypotonic and excess water

Front 57

Symptoms of hyponatremia

Back 57

2/2 cerebral edema

Nausea
Malaise
HA
Lethargy
Decreased consciousness
Seizures
Coma

Front 58

Cause of iso/hyper osmolar hyponatremia

Back 58

Hyperglycemia (1.6-4 drop for every 100 rise)
Iatrogenic (glycine, sorbital, mannitol)

Front 59

Pseudohypernatremia

Back 59

Hyperproteinemia, hyperlipidemia lead to falsely negative results

Na in aqueous soln is same, but being divided by larger vol

A problem in calculation but not in body's sensation of sodium

Front 60

Causes of hypoosmolar hypernatremia

Back 60

Water retention

ADH independent -- kidneys excretory capacity exceeded

ADH dependent -- decreased ECV, SIADH

Front 61

Low ADH hyponatremia

Back 61

Polydipsia
Inadequate solutes (tea and toast, beer)
Renal failure

Front 62

ADH regulation

Back 62

Osmolarity

Large changes in ECV

Front 63

Renal failure effect on water excretion

Back 63

Can excrete 10% of GFR

With reduced GFR, can easily be overcome by intake

Front 64

Maximum water excretion by normal kidney

Back 64

14-18L/day

Really determined drinkers can overcome that

Front 65

Normal osmolar excretion

Back 65

600 msom/daily

Mostly Na/K, urea from protein breakdown

Just carbs does not make osmoles

Front 66

Maximal dilute of urine

Back 66

50 mOsm/L

Need that much to excrete a liter

Front 67

How does ECV get low?

Back 67

True volume depletion
Diuretic therapy
Edematous states
Hypothyroid, Hypoadrenal

Front 68

When does hyponatremia not matter?

Back 68

Reset osmostat
Lower ADH setpoint than normals

No other abnormalities
No treatment effective or needed

Front 69

Thiazide induced hyponatremia

Back 69

Thiazides block Na reabsorption in PCT (reducing diluting ability)
Resulting volume depletion results in increased ADH

Lose salt, keep water -- hyponatremia

Front 70

Decreased ECV diseases

Back 70

CHF - venous pooling
Cirrhosis - venous poolnig
Nephrotic syndrome - interstitial pooling
Systemic Inflammatory Response Syndrome

Front 71

Hyponatremia from decreased ECV

Back 71

Appropriate elevation in ADH via volume stimulus
Retention of water and salt (aldosterone)
Often a disproportionate amt of water
Edema and hyponatremia

Urine osm are high

Front 72

Hypoadrenalism and hyponatremia

Back 72

Low cortisol - low CO - low ECV
Low aldosterone - inability retain Na

ADH stimulated

Urine osmoles unpredicatable 2/2 lack of aldo

Front 73

Hypothyroidism and hyponatremia

Back 73

Hypothyroidism reduces CO
Lowered ECV
ADH increased

Front 74

SIADH

Back 74

Syndrome of inappropriate ADH secretion

Euvolemic, hyposomolar hyponatremia

Urine Na > 40
Cr low or normal
Urica acid usually low

Front 75

Causes of SIADH

Back 75

CNS pathology (tumor, infection)
Pulmonary disease
small cell lung cancer
Pain
Nausea
Post-op state
Narcotics
HIV/AIDS

Drugs: SSRIs, neuroleptics, anticonvulsants, chemo, antidepressants

Front 76

Euvolemia hyponatremia

Back 76

SIADH
Hypoadrenalism
Hypothyroidism

Front 77

Problem with correcting hyponatremia too quickly?

Back 77

Ostmotic demyelination

Presents as focal neurologic deficits
2-6 days after rapid sodium correction

dysarthria, dysphagia, paresis, lethargy, coma

Front 78

How fast can you correct hyponatremia

Back 78

8 mEq/L/d

0.5 mEq/L/hr if not symptomatic
1-2 mEq/L/hr initially if symptomatic

Front 79

How to correct hyponatremia

Back 79

Water restriction
V2 receptor antagonists
Na+ supplementation
suppress ADH
overwhelm the concentrating ability of kidney

Front 80

Water restriction

Back 80

Less in than out
Use in hypervolemic patients

800-1500 cc/day allowed is typical

Front 81

What are the V2 receptor antagonists?

Back 81

Vaptans : conviaptan, topovaptan

Useful in primary SIADH, CHF, cirrhosis
Long term use not yet shown

Front 82

When is NS helpful in hyponatremia?

Back 82

Tea/Toast -- provides osmoles allowing for water diuresis

Hypovolemia

Front 83

When is NS harmful in hyponatremia

Back 83

Edematous states

SIADH

Front 84

Treating SIADH acutely

Back 84

Fluid restriction for asymptomatic patients
3% saline for severely symptomatic

Not NS

Front 85

Indications for rapid correction of hyponatremia

Back 85

Severe neurologic symptoms (seizures, coma, lethargy, MS changes, severe HA)

Known rapid onset

Front 86

Estimating instantaneous change in Na

Back 86

change = (Osm of fluid - Serum sodium)/(TBW+1)

Front 87

What do you do after you rapidly correct a patients hyponatremia?

Back 87

Monitor!

As soon as target is reached, stop

If Na continues to rise, give NS or 1/2NS

Front 88

Treating SIADH chronically

Back 88

Reduced water intake
High salt intake
Demeclocycline can be used to induce nephrogenic DI

Probably vaptans in the future

Front 89

Hypovolemia signs

Back 89

hypotension
tachycardia

Front 90

Hypovolemia effects

Back 90

Increase in RAA
ADH

Front 91

Renal causes of hypovolemia

Back 91

Sodium wasting from kidney

Usually caused by diuretics (esp thiazide)

Osmotic diuresis - hyperglycemia
Rare genetics

Front 92

Hypovolemia response electrolyte SEs

Back 92

Aldosterone related
K wasting and H wasting

Hypokalemia and metabolic alkalosis

Front 93

Urine in hypovolemia

Back 93

Low sodium (<20 mEq/L)
High osmolarity (above serum)

Fractional excretion of sodium low

Front 94

Pathogenesis of edematous states

Back 94

Excessive Na and fluid retention
Decreased ECV -- aldo/ADH

Venous HTN/hypoalbuminemia push fluid into interstitium

Front 95

Cardiorenal syndrome

Back 95

Renal failure in CHF

Reduced CO = reduced ECV

Front 96

CIrrhosis edema pathogenesis

Back 96

Increased portal venous pressure leads to third spacing

Decreased protein synthesis = hypoalbuminemia = reduced vascular oncotic pressure

Front 97

Nephrotic syndrome leads to edema?

Back 97

Increased capillary permeability
Results in interstitial leakage
and protein loss in urine
which reduces oncotic pressure
Worsening interstitial loss

ADH/aldo activated

Front 98

SIRS and edema

Back 98

Inflammatory mediators increase capillary permeability