13. body fluid osmolality Flashcards

1
Q

What helps maintain maintain medullary hyper-tonicity?

A

slow flow of vasa recta

urea recycling

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2
Q

Where are osmoreceptors located?

A

hypothalamus - Specifically in the OVLT (Organum Vasculosum of the Lamina Terminalis)

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3
Q

Where is ADH produced? Where is it released from?

A

Supraoptic nucleus of hypothalamus. Released posterior pituitary gland

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4
Q

What type of hormone is ADH?

A

peptide hormone

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5
Q

what triggers ADH release?

A

Increased osmolality

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6
Q

What does an increase in ADH result in?

A
  • Reduced water excretion (V2 receptor- mediated)

* Blood vessel vasoconstriction (V1 receptor-mediated)

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7
Q

How does ADH increase H20 reabsorption

A

• ADH causes intracellular aquaporins to fuse with the
luminal membrane.
• ADH binds to V2 receptors on the basal membrane.
• G-protein-coupled receptors, when activated, cause fusion of inactive aquaporin 2 vesicles with the membrane.
• Creates a channel through with water can
pass
• Passive flow of water

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8
Q

What are the 2 response pathways of osmoreceptors?

A

Concentration of urine and Thirst

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9
Q

summarise the two pathways of regulation of osmolality

A

Changes in Plasma osmolarity → Hypothalamic Osmoreceptors→(1) ADH → reduced Renal Water Excretion

Changes in Plasma osmolarity→Hypothalamic Osmoreceptors →(2) Thirst → increased Water intake

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10
Q

WHat does decrease in osmolarity do to ADH release?

A

• ↓ osmolarity inhibits ADH secretion =
diuresis
• Negative feedback loops that begin within
the anterior hypothalamus
• Result is a feedback loop which stabilizes
osmolarity

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11
Q

Describe the role blood pressure has on ADH

A

Increase in BP: shallow slope - needs a larger increase in osmolarity to initiate ADH release

Decrease in BP: steep slope - allows a smaller increase in osmolarity to initiate ADH release

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12
Q

Which is more important in a haemorrhage (ie volume drops) - correcting volume or osmolarity? How does ADH respond to this?

A

Volume because don’t want to have to wait for osmolality to increase fo r ADH to be naturally released (to increase H20 reabs + therefore blood volume).

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13
Q

Kidney can’t fully compensate for decreased water intake or increased salt intake so how does the body ensure we restore fluid levels?

A

Aldosterone simulates thirst centres in brain, which induce thirst by increasing plasma osmalality. We feel thirsty and drink water until we’ve consumed enough to bring plasma osmalality back to normal (stop feeling thirsty).

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14
Q

What is diabetes insipidus?

A

Failure to secrete ADH or respond to ADH, leading to inability to reabsorb water from distal part of the nephron.

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15
Q

what are the 2 types of diabetes insipidus?

A
  • Nephrogenic

* Central

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16
Q

Symptoms of diabetes insipidus?

A

polyuria, polydipsia, low urine osmolality (ie dilute urine)

17
Q

What is central diabetes insipidus?

A

Low plasma ADH due to damage to hypothalamus or pituitary gland.
• Impaired ADH synthesis or secretion by the hypothalamus

18
Q

What could cause central diabetes insipidus?

A
  • a brain injury, particularly a fracture of the base of the skull
  • a tumour
  • sarcoidosis or tuberculosis
  • an aneurysm
  • some forms of encephalitis or meningitis
19
Q

how is central diabetes insipidus treated?

A

• Treated by administering ADH (desmopressin)

Managed clinically by ADH injections or by ADH nasal spray treatments

20
Q

What is nephrogenic diabetes insipidus?

A

Acquired insensitivity of the kidney to ADH

21
Q

how is nephrogenic diabetes insipidus treated?

A
  • Difficult to managed clinically but a low-salt, low-protein diet reduces urine output.
  • No current treatment to correct the deficit
  • Thiazides can have some effect to ↑Na+ excretion
22
Q

What could cause nephrogenic diabetes insipidus?

A

Mutations in gene coding for V2 receptors, chronic pyelonephritis, polycystic kidneys or drugs such as lithium

23
Q

What is SIADH?

A

syndrome of inappropriate antidiuretic hormone

- excess release of ADH from PP or ectopic source

24
Q

What is SIADH characterised by?

A
  • Dilutional hyponatremia
  • In which the plasma sodium concentration is lowered
  • Total body fluid is increased
25
Q

what can cause SIADH?

A
  • CNS disorders e.g. stroke, abscesses
  • Malignancy
  • Lung diseases
  • Drugs e.g. opiates
  • Metabolic disease e.g. porphyria, hypothyroidism
26
Q

what are the symptoms of SIADH?

A
  • Hyponatremia and low plasma osmolality
  • Inappropriate urine osmolalitym (concentration higher than normal)
  • Inappropriate Na+ excretion (urinary [Na+] greater than 20mmol/L despite decrease in plasma Na+ concentration
27
Q

when should SIADH be considered?

A

The diagnosis should be considered in hyponatremic patients in the absence of hypovolemia, oedema,
endocrine dysfunction, renal failure and drugs, all or which can impair water excretion