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Renal > IOD Fluid and Electrolytes > Flashcards

IOD Fluid and Electrolytes Flashcards

1
Q

Hypernatremia?

A

sodium gain or water loss

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2
Q

Hyponatremia?

A

Sodium loss or water gain

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3
Q

What determines thirst?

A

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

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4
Q

Water intake and output?

A 
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
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5
Q

Osmotic pressure?

A

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

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6
Q

ADH?

A

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

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7
Q

Factors of ADH secretion?

A

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)

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8
Q

main factor of adh?

A

ecf vol

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9
Q

responses to water deficiency?

A

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

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10
Q

Sodium intake vs excretion?

A 
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
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11
Q

Renal sodium absorption?

A

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

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12
Q

How much Sodium is reabsorbed renally?

A

95-98%

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13
Q

sodium balance

A 
Blood pressure/volume sensed-
Baroreceptors-
Renal perfusion pressure
Aldosterone produced-
Adrenal cortex
Action at Kidney-
Sodium reabsorption
Loss of H+/K+
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14
Q

Important sodium values?

A

ref range-135-145 mmol/L

Life threatening-<115 >160 mmol/L

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15
Q

Assessing pts with fluid and electrolyte disturbances?

A 
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
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16
Q

urea and creatinine?

A

Urea up a lot = dehydration

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17
Q

serum osmolality

A

Indicates if other osmotically active substances are present

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18
Q

urinary sodium?

A

<20 mmol/L = conservation

>20 mmol/L = loss

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19
Q

urine/serum osmolality?

A

> 1 = water conservation

< 1 = water loss

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20
Q

when another molecule is present?

A

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

21
Q

Potassium?

A

Mostly excreted

22
Q

increased IC factors?

A

insulin-stimulates ATPase
B receptors
alkalosis

23
Q

decreased IC factors?

A

a receptors
acidosis
osmolality-leakage

24
Q

how is H linked to K?

A

pump exchanges H in and K out of cells in acidosis

Acidosis & Hyperkalaemia
Alkalosis & Hypokalaemia

25
Q

Renal control of K?

A

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

26
Q

increased intake of K?

A 
parenteral
acidosis
low insulin
tissue damage
artefactual
27
Q

decreased loss?

A 
Reduced GFR
Reduced tubular loss (potassium 
      sparing diuretics
      anti-inflammatories, ACEIs, 
      mineralocorticoid deficiency
28
Q

increased loss?

A 
Gut (diarrhoea, laxatives)
Kidney (diuretics, 
      magnesium deficiency, 
      mineralocorticoid XS
      renal tubular abnormalities)
alkalosis
insulin
B agonists
29
Q

decreased intake?

A

alcohol

anorexia

30
Q

artefact causes

A

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

31
Q

types of hyponatremia?

A 
Hypertonic hyponatraemia  - glu
(high plasma osmolality)
Hypotonic hyponatraemia :   volume status
(low plasma osmolality)
PseudohypoNa -  trigs   protein
(normal plasma osmolality)
32
Q

Hypovolaemia?

A

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

33
Q

causes of extra renal salt loss?

A 
GI loss 
(replacement with hypotonic fluid)
Vomiting
Diarrhoea
Skin loss
Burns
sweating
Haemorrhage
34
Q

renal salt loss causes?

A 
Addison’s
Diuretic Rx  
Salt losing nephritis
Solute diuresis
Cerebral Salt wasting
35
Q

euvolaemia?

A 
urine o more than 20-
Acute H20
overload
XS intake
urine o less than 20-
Chronic H20 
overload
Impaired excretion
36
Q

Acute H20
overload
XS intake causes?

A

Psychogenic
Beer potomania
Iatrogenic

37
Q

Chronic H20
overload
Impaired excretion causes?

A

SIADH Hypothyroid

Glucocorticoid deficiency

38
Q

hypervolaemia?

A

urine o less than 20-oedema

39
Q

oedema causes?

A

Cirrhosis Cardiac failure Nephrotic syndrome

usually + diuretic Rx

40
Q

Control of sodium?

A

IV vol control-RAAS

41
Q

SIADH

A

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

42
Q

drugs increasing ADH?

A

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

43
Q

drugs potentiate ADH?

A

Tricyclics
SSRI’s : Prozac
Paracetamol
Indomethacin

44
Q

Diuretics?

A

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

45
Q

ineffective plasma vol causes?

A 
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
46
Q

Sodium can be found in?

A

Antibiotics and IV fluids

colloid (gelofusine and haemacel) and crystalloids (Hartmanns and saline)

47
Q

Distribution of IV fluids?

A

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

48
Q

hyponatremia management issues?

A

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

49
Q

hypernatremia management issues?

A

over rapid correction leads to cerebral oedema

water into plasma and csf into cells but witholding sodium causes water movement into cells-swelling

Renal (14 decks)

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