IOD Fluid and Electrolytes

Question 1

Hypernatremia?

Answer 1

sodium gain or water loss

Question 2

Hyponatremia?

Answer 2

Sodium loss or water gain

Question 3

What determines thirst?

Answer 3

osmoreceptors-changes i ECM
Low pressure baroreceptors-great veins and RA of heart
High pressure-carotid sinus and aorta
Ang ii –renin-renal hypotension

Question 4

Water intake and output?

Answer 4

Intake
Dietary intake (Thirst)
Output 
Obligatory losses
Skin
Lungs
Controlled losses – these depend on:
Renal function
Gut (main role of the colon)
Vasopressin/ADH (anti-diuretic hormone)
Redistribution

Question 5

Osmotic pressure?

Answer 5

Osmotically active substances in the blood may result in water redistribution to maintain osmotic balance but cause changes in other measured solutes
hyperosmolality-cells shrink
hyposmolality-cells swell

Question 6

ADH?

Answer 6

ADH acts on renal collecting ducts to make them permeable to water
allows free water absorption and production of a concentrated urine controlling ECF osmolality
only ADH concs urine

Question 7

Factors of ADH secretion?

Answer 7

Secretion stimulated by:
Increase in plasma osmolality (v. sensitive 1-2% change)
Pain, stress, nausea, drugs, lung and CNS lesions, ectopic
Decrease in plasma volume (>5-8%)
Secretion decreased by:
Decrease in plasma osmolality (plasma dilution)
Increase in plasma volume
Ethanol (resulting in diuresis)

Question 8

main factor of adh?

Answer 8

ecf vol

Question 9

responses to water deficiency?

Answer 9

high ECF osmolality
ADH-renal water retention
HT thirst centre-increased water-restoration of ECF
redistribution of water from ICF-increased ECF water

Question 10

Sodium intake vs excretion?

Answer 10

Intake
Dietary (unless vegan do not add salt)
Western diet 100-200 mmol/day
Output
Obligatory loss
Skin
Controlled excretion
Kidneys     
Aldosterone
GFR
Gut - most sodium is reabsorbed; loss is pathological

Question 11

Renal sodium absorption?

Answer 11

PCT-most sodium reabsorbed, increases as sodium reabsorption does, water absorbed is isoosmotic
loop of henle-just sodium
DCT-secretion of K and H
RAAS-increases sodium reabsorption

Question 12

How much Sodium is reabsorbed renally?

Answer 12

95-98%

Question 13

sodium balance

Answer 13

Blood pressure/volume sensed-
Baroreceptors-
Renal perfusion pressure
Aldosterone produced-
Adrenal cortex
Action at Kidney-
Sodium reabsorption
Loss of H+/K+

Question 14

Important sodium values?

Answer 14

ref range-135-145 mmol/L

Life threatening-<115 >160 mmol/L

Question 15

Assessing pts with fluid and electrolyte disturbances?

Answer 15

History
Fluid intake / output
Vomiting/diarrhoea
Past history
Medication

Examination - Assess volume status
Lying and standing BP
Pulse
Oedema
Skin turgor/Tongue
JVP / CVP
fluid chart

Question 16

urea and creatinine?

Answer 16

Urea up a lot = dehydration

Question 17

serum osmolality

Answer 17

Indicates if other osmotically active substances are present

Question 18

urinary sodium?

Answer 18

<20 mmol/L = conservation

>20 mmol/L = loss

Question 19

urine/serum osmolality?

Answer 19

> 1 = water conservation

< 1 = water loss

Question 20

when another molecule is present?

Answer 20

Calculated Serum osmolality = 2 x Na + urea + glucose (+/- 10)
5 for u and g if unknown
move water out of cells to balance osmolality so seems like hyponatremia but amount of sodium is the same

Question 21

Potassium?

Answer 21

Mostly excreted

Question 22

increased IC factors?

Answer 22

insulin-stimulates ATPase
B receptors
alkalosis

Question 23

decreased IC factors?

Answer 23

a receptors
acidosis
osmolality-leakage

Question 24

how is H linked to K?

Answer 24

pump exchanges H in and K out of cells in acidosis

Acidosis & Hyperkalaemia
Alkalosis & Hypokalaemia

Question 25

Renal control of K?

Answer 25

Most K absorbed in PCT and LoH Control in DCT and CD aldosterone causes pump of sodium into cells linig tubule-depolarisation so K into tubule lumen

Question 26

increased intake of K?

Answer 26

``` parenteral acidosis low insulin tissue damage artefactual ```

Question 27

decreased loss?

Answer 27

``` Reduced GFR Reduced tubular loss (potassium sparing diuretics anti-inflammatories, ACEIs, mineralocorticoid deficiency ```

Question 28

increased loss?

Answer 28

``` Gut (diarrhoea, laxatives) Kidney (diuretics, magnesium deficiency, mineralocorticoid XS renal tubular abnormalities) alkalosis insulin B agonists ```

Question 29

decreased intake?

Answer 29

alcohol | anorexia

Question 30

artefact causes

Answer 30

Not using vacutainers Narrow needles Injecting blood through narrow needles into vacutainers cause cell rupture or high EDTA/Mg levels increase K levels

Question 31

types of hyponatremia?

Answer 31

``` Hypertonic hyponatraemia - glu (high plasma osmolality) Hypotonic hyponatraemia : volume status (low plasma osmolality) PseudohypoNa - trigs protein (normal plasma osmolality) ```

Question 32

Hypovolaemia?

Answer 32

urine more than 20- extra-renal salt loss urine o less than 20-renal salt loss

Question 33

causes of extra renal salt loss?

Answer 33

``` GI loss (replacement with hypotonic fluid) Vomiting Diarrhoea Skin loss Burns sweating Haemorrhage ```

Question 34

renal salt loss causes?

Answer 34

``` Addison’s Diuretic Rx Salt losing nephritis Solute diuresis Cerebral Salt wasting ```

Question 35

euvolaemia?

Answer 35

``` urine o more than 20- Acute H20 overload XS intake urine o less than 20- Chronic H20 overload Impaired excretion ```

Question 36

Acute H20 overload XS intake causes?

Answer 36

Psychogenic Beer potomania Iatrogenic

Question 37

Chronic H20 overload Impaired excretion causes?

Answer 37

SIADH Hypothyroid | Glucocorticoid deficiency

Question 38

hypervolaemia?

Answer 38

urine o less than 20-oedema

Question 39

oedema causes?

Answer 39

Cirrhosis Cardiac failure Nephrotic syndrome | usually + diuretic Rx

Question 40

Control of sodium?

Answer 40

IV vol control-RAAS

Question 41

SIADH

Answer 41

Euvolaemia ie. no evidence of volume depletion or oedema Hyponatraemia and hypo-osmolality Inappropriately high urine osmolality & excessive renal excretion of Na Normal renal, adrenal, pituitary, thyroid Not on any drugs (diuretics, antidiuretics) DIAGNOSIS OF EXCLUSION !! Clinical and biochemical improvement with fluid restriction causes-Small cell carcinoma, TB or pneumonia

Question 42

drugs increasing ADH?

Answer 42

Anticonvulsants : carbamazepine Antineoplastics : cyclophosphamide Hypoglycaemics : chlorpropamide Narcotics : morphine

Question 43

drugs potentiate ADH?

Answer 43

Tricyclics SSRI’s : Prozac Paracetamol Indomethacin

Question 44

Diuretics?

Answer 44

Thiazides, frusemide, K+ sparing (amiloride, spironolactone)

Question 45

ineffective plasma vol causes?

Answer 45

``` low albumin diuretics increased fluid loss-oedema, ascites, facial oedema RAAS- sodium retention portal hypertension and splanchnic VD thirst water from ICF ADH -volume overrides osmolar controls so increased water hypovolaemic dilutional hyponatremia ```

Question 46

Sodium can be found in?

Answer 46

Antibiotics and IV fluids | colloid (gelofusine and haemacel) and crystalloids (Hartmanns and saline)

Question 47

Distribution of IV fluids?

Answer 47

colloid-plasma saline/balanced crystalloids-interstitial and lymphatic sodium chloride and glucose-IC and all glucose-IC and all

Question 48

hyponatremia management issues?

Answer 48

Over-rapid correction may lead to central pontine myelinolysis-rapid sodium uptake causes water movement out of cells so myelin destoyed-lockedin or death

Question 49

hypernatremia management issues?

Answer 49

over rapid correction leads to cerebral oedema | water into plasma and csf into cells but witholding sodium causes water movement into cells-swelling