Renal Physiology: Salt and water Flashcards

1
Q

More adept breakdown of ECF

note 70kg male, 60% water (42L) so 2/3 ICF, 1/3 ECF

A

IF, transcellular, intravascular

Transcellular (CSF, aqueous humour, synovial fluid, pericardial/pleural). Formed from transport activities of cells.

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2
Q

Key electrolyte concs

A

ECF: high sodium, low potassium
ICF: low sodium, high potassium

Maintained by Na+/K+ ATPase

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3
Q

What is plasma osmolarity maintained between, and what is it regulated by

NB tonicity

A

285-295 mOsmol/L
Regulated by salt and water
Hyperosmolar is too much cation, too little water
Hypo-osmolar is too little cation, too much water

effect a solution has on a cell, e.g hypertonic, cell shrinks

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4
Q
Brief definition of what occurs at each part of nephron
Glomerulus
PCT
LoH: A+ D
DCT
CD

note on filtrate osmolarity at different points

A

Glomerulus: free filtration of water and salt
PCT: 65-75% of water and sodium reabsorbed, slight filtrate concentration to 300mOsmol/L
LoH, descending: Active water reabsorption
LoH, ascending: Active Na+ reabsorption, 15-20%
(At bottom, 600mOsmol/L, by top 400)
DCT: 5% Na+
CD: 5% Na+

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5
Q

brief diuretics, thiazides and loop

A

Thiazides, in DCT inducing natriuresis (sodium, chloride symport)
Loop, acting at LoH (NKCCl)
Amiloride, ENaC ?

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6
Q

When is ADH secreted

A

Low BP/BV, or increase in osmolarity
Increases water reabsorption, increases BP and lowers osmolarity.
Concentrates urine
Upregulate aquaporins

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7
Q

Aldosterone, when is it excreted, where it acts, effects

A

Stimulated by increased K+ or A2, mineralocorticoid acting on DCT/CD
Increases Na+ reabsorption (holds onto water), increases potassium excretion, up regulates Na+/K+ ATPase activity

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8
Q

RAAS

A

Renin produced in response to, low renal BF/GFR, macula densa sense low Na+, sympathetic tone
A2: VC, thirst, increase ADH/aldosterone; increase sodium reabsorption (PCT). Raises GFR (efferent arteriole contriction) lowers by mesangial cell contraction??

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9
Q

Hypernatraemia

causes of

A

> 145mmol/L
Too much salt/volume depletion(water only):
Impaired thirst/consciousness, so common in hospital
No access to fluids
Large water loss
Solute diuresis, such as in DKA. Hypoglycaemia induced diuresis, where water is lost but normal sodium.

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10
Q

Diabetes insipidus, cause of hypernatraemia

results in?

A

Reduced amount or efficacy of ADH
Results in polyuria and water loss (dilute urine)
Patient can not drink enough to keep up with losses.
Results in hypernatraemia, elevated plasma osmolarity

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11
Q

Types of DI

A

Central: most from brain injury/trauma, abnormal production. Can give analogues (intranasal/IM)
Nephrogenic: partial/complete ADH resistance, defective aquaporin channels, drug toxicity such as amiloride

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12
Q

Two common causes of hyponatraemia

A

Excessive Na+ loss or water retention

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13
Q

Pseudohyponataemia
How to check
causes

A

When Na+ is falsely low, as serum osmolarity will be normal. Normal osmolarity
Causes:
-Hyperglycaemia: an osmotic water shift into blood stream, artifically lowering [Na+], or with mannitol infusion
-Hyperlipidaemia/hyperproteinaemia

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14
Q

Step one when checking hyponatraemic pateint

A

Check urine osmolality

  • If less than 100mOsmol/kg, very dilute urine (low salt)
  • Due to polydipsia,water intoxication. DDx with psychotropic drugs, schizophrenia, beer potomania
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15
Q

Step two in checking hyponatraemic patient

A

VOLUME STATUS

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16
Q

Hypovolemic patinnt with hyponatraemia

learnt the examples

A

Dehydrated, water loss and sodium loss
Check urine Na+, if low
-Sodium loss, relatively less water loss such as in: diarrhoea, vomiting, bowel obstruction, skin losses (sweating, burns); urinary losses (diuretics, Addisons, ketonuria, osmotic diuresis)

17
Q

Hypervolemic pateint with hyponatraemia

A

Fluid overloaded, too much water!
Sodium is retained, but more water is than sodium!
Cirrhosis, nephrotic syndrome, HF/RF

18
Q

Euvolemic patient with hyponatraemia

A

Endocrinopathies: hypothyroid, low cortisol
SIADH
Diuretics
fluid replacement

19
Q

SIADH

urine tests show

A
  • Inappropriate secretion of ADH in absence of normal stimuli such as low BP or increased osmolarity
  • Body accumulates too much water, which is stored in cells, thus euvolemic
  • Urine osmolarity is not low, neither is sodium
  • Plasma osmolality is low

Causes: head trauma, surgery, tumours (lung), chronic lung disease, SSRI’s

Treat with fluid restriction

20
Q

Hyponatraemia symptoms

A
Slow onset (brain adaptation): confusion, not quite self
Rapid onset: cerebral oedema, confusion and seizures, coma

Brain adaptation to cerebral oedema due to water gain occurs over time, so treatment must be in consideration. Correction speed= onset speed

21
Q

Hyponatraemia treatments

A

Slow onset: gradual, fluid restriction only (no more than 8mmol/L a day)
Rapid onset: vigorous treatment, fluid restriction, normal saline or 3% saline in ICU

22
Q

Consequence of rapid treatment in hyponatraemia

A

If patient has cerebral oedema, and done too rapidly, not over time for brain adaptation, can cause central pontine myelosis
Compression of myelin sheaths, quadraparesis, pseudobulbar palsy (can’t control facial movements), locked in syndrome (body/facial paralysis, but conscious+ eye movements)