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Year 2 RE > Physiology of Thirst and Fluid Balance and its Disorders > Flashcards

Physiology of Thirst and Fluid Balance and its Disorders Flashcards

1
Q

What is the difference between osmolality and osmolarity?

A
  • osmolality = solute concentration is osmoles of solute/kg of solution
  • osmolarity = solute concentration in osmoles of solute per litre of solution
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2
Q

What can happen to a cell if there is an increased extracellular (outside the cell) osmolality?

A
  • H2O leaves the cell to dilute the high extracellular (outside the cell) osmolality
  • the cell becomes dehydrated
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3
Q

What can happen to a cell if there is an increased intracellular (inside the cell) osmolality?

A
  • H2O enters the cell to dilute the high intracellular (inside the cell) osmolality
  • the cell becomes swollen and edema occurs
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4
Q

How does the body detect when there is change in the osmolality in the plasma?

A
  • osmoreceptors located in the anterior hypothalamus on the wall of the 3rd ventricle
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5
Q

If we lose H2O due to sweat or we eat a really salty meal, the extracellular (outside the cell) osmolality will increase, stimulating the osmoreceptors located in the anterior wall of the 3rd ventricle and the the anterior hypothalamus. What is this cluster of nuclei in the hypothalamus called?

A
  • supraoptic nuclei
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6
Q

If we lose H2O due to sweat or we eat a really salty meal, the extracellular (outside the cell) osmolality (ECO) will increase, stimulating the osmoreceptors located in the anterior wall of the 3rd ventricle and the the anterior hypothalamus. This cluster of nuclei in the hypothalamus is called the supraoptic nuclei. When they detect the increased ECO what happens?

A
  • stimulate the hypothalamus that stimulates the posterior pituitary gland
  • posterior pituitary gland then releases anti-diuretic hormone (ADH) (vasopressin)
  • ADH retains H2O through kidneys and vasoconstricts blood vessels
  • the body also instigates thirst to consume more H2O
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7
Q

What is the normal plasma osmolality range?

A
  • 285 and 295 mosmol/kg.
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8
Q

When extracellular osmolality increases, due to fluid loss, the sensation of thirst is stimulated and there is a release of anti-diuretic hormone (ADH). What 2 parts of the brain are involved in this response?

A
  • thirst = cerebral cortex

- ADH = hypothalamus

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9
Q

What happens to thirst and anti-diuretic hormone release in the presence of:

  • high plasma osmolality (lots of solutes in blood)
  • low plasma osmolality (fewer solutes in blood)
A
  • high plasma osmolality = thirst and ADH release

- low plasma osmolality = no thirst and no ADH release

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10
Q

The posterior pituitary gland is unable to synthesise anti-diuretic hormone (ADH), meaning the hypothalamus must synthesise this and transport it to the posterior pituitary gland for release into the blood. What are the 2 nuclei in the hypothalamus that synthesise ADH?

A
  • paraventricular nuclei

- supraoptic nuclei

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11
Q

What are magnocellular cells, also called M cells?

A
  • neurons with large cell bodies
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12
Q

Magnocellular cells, or M cells are synthesised in paraventricular and supraoptic nuclei at the base of the hypothalamus. What happens to the synthesised anti-diuretic hormone (ADH) once it has been synthesised?

A
  • packed into vesicles in the cell body of magnocellular (M) neurons
  • these neurons travel along the pituitary stalk to the posterior pituitary gland
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13
Q

What cation is required for the release of packed anti-diuretic hormone in vesicles to be released into the posterior pituitary gland and then into the blood?

A
  • Ca2+
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14
Q

Anti-diuretic hormone is able to increase fluid retention in the kidneys. How does it increase fluid retention?

A
  • prevents diuresis (passing of urine)

- retains the fluid

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15
Q

What 3 areas in the kidney is anti-diuretic hormone able to have an effect and increase H2O retention? Label the image with the labels below:

distal tubule
collecting tubule
collecting duct epithelia

A

1 - distal tubule
2 - collecting tubule
3 - collecting duct

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16
Q

Anti-diuretic hormone able to increase water retention in the kidneys. What does ADH bind with in the kidneys?

A
  • vasopressin receptor 2 (AVPR2)
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17
Q

Anti-diuretic hormone (ADH) able to increase water retention in the kidneys. ADH is able to bind with vasopressin receptor 2 (AVPR2). What type of membrane receptor is this and what does this trigger intracellularly?

A
  • GPCR, specifically Gas
  • ATP is converted into cAMP
  • cAMP activates protein kinase A (PKa)
  • PKa increases phosphorylation
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18
Q

Anti-diuretic hormone (ADH) able to increase water retention in the kidneys. ADH is able to bind with vasopressin receptor 2 (AVPR2), a GPCR, specifically Gas. This activates protein kinase A (PKa) and increases phosphorylation. What does this then cause an increase in on the cell membrane on the tubular surface?

A
  • increased synthesis of water channel proteins called aquaporin 2 (AQP-2)
  • vesicles containing AQP-2 bind with the cell membrane
  • H2O can move from the lumen and back into the blood through AQP-3 and 4 on basolateral membrane
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19
Q

What does polyuria mean?

A
  • poly = lots of
  • uria = urine
  • production of lots of urine
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20
Q

What does polydipsia mean?

A
  • poly = lots of

- dipsia = greek for thirst

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21
Q

What effect does polyuria and polydipsia have on plasma osmolality?

A
  • polyuria = excessive passing of urine = increase of plasma osmolality
  • polydipsia = excessive thirst and water consumption = decrease of plasma osmolality
22
Q

If a patient presents with polyuria and/or polydipsia, what is the first disease and secondary effects that must be ruled out?

A
  • diabetes mellitus

- hypercalcaemia and hypokalaemia

23
Q

What does diabetes insipidus mean?

A
  • diabetes = relates to passing of a lot of urine
  • insipidus = tasteless
  • essentially passing of very diluted/tasteless urine
24
Q

In diabetes insipidus (DI), is plasma osmolality high or low?

A
  • high plasma osmolality
  • DI is characterised by excessive fluid loss
  • excessive fluid loss will therefore increase plasma osmolality
25
Q

To be diagnosed with diabetes insipidus, how much fluid must a patient pass in 1 day?

A
  • 3L/day

- patients need to document fluid intake

26
Q

Central diabetes insipidus (CDI) is a rare disorder that can cause polydipsia (excessive thirst) and polyuria (excessive tasteless urine, no sugar like in diabetes mellitus). What is CDI?

A
  • problem is located centrally in the hypothalamus or pituitary gland reducing anti-diuretic hormone (ADH)
  • reduced ADH reduces vasoconstriction of blood vessels and reduced H2O retention in kidneys
  • means patient would pass a lot of urine
27
Q

Central diabetes insipidus (CDI) is a rare disorder that can cause polydipsia and polyuria. What are the main causes of this?

A
  • idiopathic = 27%
  • head trauma or neurosurgery that damage can be in hypothalamus osmoreceptors, supraoptic nucleus, or the supraoptico-hypophysial tract
  • genetic (5%)
  • pituitary tumour (no ADH released)
28
Q

Nephrogenic diabetes insipidus (DI) is a rare disorder that can cause polydipsia (excessive thirst) and polyuria (excessive tasteless urination, no sugar like in diabetes mellitus). What is this and what causes this?

A
  • damage to the nephron in the kidneys
  • unresponsive to anti-diuretic hormone (ADH)
  • most common causes include genetic disorder, medications (lithium) and kidney disease
29
Q

Nephrogenic diabetes insipidus (DI) is a rare disorder that can cause polydipsia and polyuria. This is caused by damage to the nephron in the kidneys, reducing their responsive to anti-diuretic hormone (ADH). What are the main causes of this?

A
  • genetic disorder (V2 encoding gene)
  • medications (lithium)
  • kidney disease
  • persistance hypercalcaemia (Ca2+) and hypokalaemia (K+)
30
Q

Dipsogenic diabetes insipidus (DI) is a rare disorder that can cause polydipsia (excessive thirst) and polyuria (excessive tasteless urine, unlike in diabetes mellitus where glucose is present). What is this and what causes this?

A
  • caused by drinking excessive amounts of H2O

- common in patients with mental disorders such as psychosis

31
Q

Dipsogenic diabetes insipidus (DI) is a rare disorder that can cause polydipsia and polyuria. It is caused by drinking excessive amounts of H2O and is common in patients with mental disorders such as psychosis. How does drinking excessive H2O cause polyuria?

A
  • excessive fluid intake lowers plasma osmolality
  • ADH secretion is reduced
  • high urine output is encouraged to increase plasma osmolality
32
Q

What is a water deprivation test?

A
  • a test which measures how your kidneys respond when you don’t have anything to drink
33
Q

A water deprivation test is a test which measures how your kidneys respond when you don’t have anything to drink. What are the 2 methods that can be used in this test?

A
  • period of dehydration with the patient

- administer synthetic vasopressin (ADH) called desmopressin

34
Q

A water deprivation test is a test which measures how your kidneys respond when you don’t have anything to drink. There are 2 methods that can be used in this test:

  • period of dehydration with the patient
  • administer synthetic vasopressin (ADH) called desmopressin

What must be measured in the patient prior to and following the test?

A
  • plasma and urine osmolality
35
Q

A water deprivation test is a test which measures how your kidneys respond when you don’t have anything to drink. There are 2 methods that can be used in this test:

  • period of dehydration with the patient
  • administer synthetic vasopressin (ADH) called desmopressin

Plasma and urine osmolality must be measured in the patient prior to and following the test. In the results, what does normal plasma osmolality and high urine osmolality indicate?

A
  • a normal response
36
Q

A water deprivation test is a test which measures how your kidneys respond when you don’t have anything to drink. There are 2 methods that can be used in this test:

  • period of dehydration with the patient
  • administer synthetic vasopressin (ADH) called desmopressin

Plasma and urine osmolality must be measured in the patient prior to and following the test. In the results, what would be the diagnosis if the patient has:

  • low urine osmolality prior to and following dehydration due to polyuria
  • following desmopressin administration, urine osmolality increases
A
  • central diabetes insipidus
  • low/no ADH being released centrally from the supraoptic nucleus and then posterior pituitary gland, meaning H2O is not retained
  • BUT if synthetic ADH (desmopressin) is administered the kidneys respond normally
37
Q

A water deprivation test is a test which measures how your kidneys respond when you don’t have anything to drink. There are 2 methods that can be used in this test:

  • period of dehydration with the patient
  • administer synthetic vasopressin (ADH) called desmopressin

Plasma and urine osmolality must be measured in the patient prior to and following the test. In the results, what would be the diagnosis if a patient has:

  • low urine osmolality prior to and following dehydration
  • following desmopressin administration, urine osmolality does not increase, or only marginally
A
  • kidneys do not respond to synthetic ADH

- nephrogenic diabetes insipidus

38
Q

A water deprivation test is a test which measures how your kidneys respond when you don’t have anything to drink. There are 2 methods that can be used in this test:

  • period of dehydration with the patient
  • administer synthetic vasopressin (ADH) called desmopressin

Plasma and urine osmolality must be measured in the patient prior to and following the test. What would the diagnosis be if the patient has:

  • a high urine osmolality following dehydration due to low urine output
  • no need to administer vasopressin
A
  • patient has primary/dipsogenic diabetes insipidus

- patient will still have a high urine osmolality and no need to administer desmopressin

39
Q

Central diabetes insipidus (CDI) is a rare disorder that can cause polydipsia and polyuria. This is due to a problem is located centrally in the hypothalamus or pituitary gland reducing anti-diuretic hormone (ADH) release, meaning reduced ADH reduces vasoconstriction of blood vessels and reduced H2O retention in kidneys. How can this be treated?

A
  • desmopressin (synthetic anti-diuretic hormone)

- can cause hyponatraemia (low Na+) IF the polydipsia is not treated (stop excessive fluid intake)

40
Q

Nephrogenic diabetes insipidus (DI) is a rare disorder that can cause polydipsia and polyuria. Caused by damage to the nephron in the kidneys, which are unresponsive to anti-diuretic hormone (ADH). The most common causes include genetic disorder, medications (lithium) and kidney disease. How can this be treated?

A
  • correct metabolic or drug cause damaging nephrons

- likely to be due to thiazide diuretics (help clear fluid from the body) / NSAIDs

41
Q

Dipsogenic diabetes insipidus (DI) is a rare disorder that can cause polydipsia and polyuria. It is caused by drinking excessive amounts of H2O and is common in patients with mental disorders such as psychosis. How can this be treated?

A
  • explanation, persuasion

- psychological therapy where required

42
Q

What is the diagnosis of hyponatraemia?

A
  • <135mmol/L of Na+
43
Q

How can hyponatraemia, where Na+ drops below 135mmol/L present in patients?

A
  • acute = asymptomatic, headache, nausea, mood change, cramps, lethargy
  • severe = confusion, drowsiness, seizures, coma
44
Q

Hyponatraemia can also be linked with patients plasma volumes. What is hypovolemia, and how can this cause hyponatraemia?

A
  • hypovolemia refers to a loss of extracellular fluid
  • can be caused by an inability of kidneys to retain H2O and Na+ due to decreased ADH
  • loss of Na+ through vomiting and/or diarrhoea means a loss of Na+, resulting in an inability of kidneys to retain H2O, increased levels of anti-diuretic hormone will be released in response
45
Q

Hyponatraemia can also be linked with patients plasma volumes. What is normovolaemia, and how can this cause hyponatraemia?

A
  • can be caused by hypoadrenalism, hypothyroidism

- inappropriate ADH secretion

46
Q

Hyponatraemia can also be linked with patients plasma volumes. What is hypervolaemia, and how can this cause hyponatraemia?

A
  • too much fluid in the body (heart or renal failure)

- decreases plasma osmolality

47
Q

If a patient presents with hyponatraemia, what must be excluded?

A
  • exclusion of ‘drug’ causes, (thiazide diuretics which remove fluid from body)
48
Q

Why must hyponatraemia be corrected slowly?

A
  • overcorrection can cause plasma oedema

- cause neural damage including oligodendrocytes and central myelinolysis

49
Q

Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is a condition in which the body makes too much antidiuretic hormone (ADH). How can patients present in relation to plasma volumes, choose one from below?

  • Hypovolaemia
  • Normovolaemia (euvolaemia)
  • Hypervolaemia
A
  • Normovolaemia (euvolaemia)
  • low plasma Na+ and low plasma osmolality
  • high urine Na+ concentration so looks normal
  • also linked with reduced aldosterone (which normally retains H2O and Na+)
50
Q

Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is a condition in which the body secretes inappropriate amounts of antidiuretic hormone (ADH). Patients present with normovolaemia (euvolaemia), BUT patients have a low plasma Na+, and low plasma osmolality and high urine Na+ concentration. What should be tested in these patients?

A
  • renal, adrenal and thyroid function
51
Q

Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is a condition in which the body makes too much antidiuretic hormone (ADH). Patients present with normovolaemia (euvolaemia), low plasma Na+ and low plasma osmolality and high urine Na+ concentration. Following tests of renal, adrenal and thyroid function, what are the 3 main ways these patients be treated?

A

1 - fluid restriction (induce negative fluid balance)
2 - demeclocycline (induces nephrogenic diabetes insipidus (non responsive to ADH)
3 - vasopressin (ADH) antagonist

Year 2 RE (53 decks)

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