Body Fluid Osmolality Flashcards

1
Q

Where are Osmoreceptors found? What do they sense?

What happens next?

A
  • In hypothalamus
  • Sense changes in plasma osmolarity

Signals secondary responses, mediated by 2 complimentary pathways;

  • Urine concentration
  • Thirst
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2
Q

Describe the Synthesis of ADH (A peptide hormone)

A
  • Made in Supraoptic nucleus of Hypothalamus

- Transported to Post. Pituitary gland and stored until release

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3
Q

What triggers ADH release?

List 3 effects of ADH

A
  • Increase in plasma osmolarity
  • Reduce water excretion (V2 receptor mediated)
  • Vasoconstriction (V1 receptor mediated)
  • Increased urea recycling through UT1 transporters
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4
Q

How does ADH reduce water excretion?

A
  • Causes intracellular aquaporins to fuse with luminal membrane
  • Binds to V2 receptors on Basal Membrane, causing fusion of inactive aquaporins
  • Creates a channel through which water flows passively
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5
Q

When is ADH secretion at zero?

What is diuresis?

How is ADH secretion regulated?

A
  • Never, always secreted but more secreted when plasma osmolarity increases
  • Loss of water
  • Negative feedback via plasma osmolarity
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6
Q

How does BP affect ADH release upon increase in plasma osmolarity?

Why is this done?

A

Low BP:
- More ADH released when osmolarity increases

High BP:
- Less ADH released when osmolarity increases

  • More important to preserve volume than osmolarity
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7
Q

What is Diabetes Insipidus?

What are 2 types of causes

A
  • Inability to reabsorb water from the distal part of the nephron
  • due to failure of Secretion/ Action of ADH
  • Central
  • Nephrogenic
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8
Q

What are 3 symptoms of Diabetes Insipidus

Insipidus means tasteless

A
  • Polyuria
  • Polydipsia
  • Low urine osmolality
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9
Q

What happens in Central Diabetes Insipidus?

List 5 causes

A
  • Impaired ADH synthesis/ secretion by Hypothalamus

Damage to hypothalamus/ pit gland due to;

  • Brain injury (Basilar skull fracture)
  • Tumour
  • Aneurysm
  • Encephalitis/ Meningitis
  • Sarcoidosis/ Tuberculosis
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10
Q

How is Central Diabetes Insipidus managed clinically and treated?

A

Treatment;
- Administering Desmopressin/ DDAVP (Artificial ADH)

Management;

  • ADH injections
  • ADH Nasal spray treatments
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11
Q

What happens in Nephrogenic Diabetes Insipidus?

There is no treatment. How can it be managed?

A
  • Acquired insensitivity of kidney to ADH

- Low salt, low protein diet to reduce urine output

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12
Q

List 4 causes of Nephrogenic Diabetes Insipidus

A
  • Mutations in gene coding for V2 receptors
  • Chronic Pyelonephritis
  • Polycystic kidneys
  • Drugs such as Lithium
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13
Q

In Nephrogenic Diabetes Insipidus, plasma ADH levels are normal.

Are there any treatments to correct the deficit?

A

No, but Thiazides can have some effect to increase Na excretion

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14
Q

What is SIADH? (Syndrome of Inappropriate ADH secretion)

What are 3 characteristics?

A
  • Excessive release of ADH from Post Pit gland or another source
  • Dilutional hyponatreamia (Appears to have low sodium, but actually has too much water)
  • Lowered plasma sodium concentration
  • Increased total body fluid
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15
Q

List 5 causes of SIADH

A
  • CNS Disorders (stroke, abscess)
  • Malignancy
  • Lung diseases
  • Drugs (opiates)
  • Metabolic diseases (Hypothyroidism, Porphyria)

(Porphyria- Liver diseases where Porphyrins accumulate in body and affect CNS)

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16
Q

List 3 symptoms of SIADH

A
  • Hyponatraemia + Low plasma osmolarity
  • Abnormal urine osmolarity
  • Abnormal Na excretion (>20mM)

Consider diagnosis in hyponatraemic patients who DON’T have hypovolaemia/ oedema/ endocrine dysfunction/ renal failure/ drugs
(These can impair H2O excretion)