Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 2 - T2 Theme 1 > L10 - Physiology of thirst and fluid balance and its disorders > Flashcards

L10 - Physiology of thirst and fluid balance and its disorders Flashcards

1
Q

Featured hormones in the physiology of thirst and fluid balance

A
  • Anti-diuretic hormone (ADH)

- Arginine vasopressin (AVP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Examples of pathophysiology - thirst and fluid balance

A
  • Polyuria and polydipsia - diabetes insipidus

- Hyponatraemia - syndrome of inappropriate ADH secretion (SIADH)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Why is regulation of water balance important

A
  • Regulation of water balance ensures plasma osmolality(and extracellular fluid osmolality) remains stable
  • Narrow range of plasma osmolality - 285-295 mosmol/kg
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

3 key determinants involved in the regulation of water balance

A
  • Antidiuretic hormone - osmotically stimulated secretion
  • Kidney - wide variation in urine output (0.5-20 L/day)
  • Thirst - osmoregulated, stimulates fluid intake
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are osmoreceptors

A
  • Groups of specialised cells which detect changes in plasma osmolality (esp sodium)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Location of osmoreceptors

A
  • Located in the anterior wall of 3rd ventricle

- Fenestrations in the blood-brain barrier allow circulating solutes(osmoles) to influence brain osmoreceptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What do osmoreceptors respond to

A
  • Osmoreceptor cells alter their volume by a transmembrane flux of water in response to changes in plasma osmolality
  • This initiates neuronal impulses that are transmitted to the hypothalamus to synthesise ADH, and to the cerebral cortex to register thirst
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is arginine vasopressin

A
  • Human form of ADH

- Nonapeptide - 9 amino acid peptide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Where is vasopressin synthesised

A
  • In neurons in supraoptic and paraventricular nuclei of the hypothalamus
  • Secretory granules migrate down axons to posterior pituitary from where AVP is released ww
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Where are AVP and copeptin released

A
  • AVP and copeptin are released into capillaries of the portal system that transport copeptin to the anterior pituitary
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Where are AVP and copeptin stored

A
  • AVP and copeptin storage occurs in axons in the posterior pituitary
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What does AVP stimulate the release of

A
  • AVP stimulates endocrine cells to release ACTH from anterior pituitary
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Receptors that mediate ADH action in the kidney

A
  • V2 receptors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Where are ADH-sensitive water channels (aquapprins) normally stored

A
  • In cytoplasmic vesicles, moves to and fuses with the luminal membrane
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Effect of ADH

A
  • Increases water permeability of renal collecting tubules, promoting water reabsorption
  • When ADH cleared, water channels removed from the luminal surface (endocytosis) and returned to cytoplasm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Effects of low plasma osmolality on osmoregulation

A
  • AVP undetectable
  • Dilute urine
  • High urine output
  • No thirst
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Effects of high plasma osmolality on osmoregulation

A
  • High AVP secretion
  • Concentrated urine
  • Low urine output
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Effect of high osmolality on thirst

A
  • Increased thirst sensation

- Drinking immediately transiently suppresses AVP secretion and thirst (avoids overshoot)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Relationship between plasma AVP and plasma osmolality/urine osmolality

A
  • Direct correlation

- Plasma vasopressin levels increase with plasma osmolality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Link between urine osmolality and plasma vasopressin levels

A
  • Urine osmolality increases with plasma vasopressin levels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Three other main causes of polyuria and polydipsia

A
  • Cranial (central) diabetes insipidus (DI) - lack of osmoregulated AVP secretion
  • Nephrogenic diabetes insipidus (DI) - lack of response of the renal tubule to AVP
  • Primary polydipsia - psychogenic polydipsia, social/cultural
    All may be ‘partial’
22
Q

What is primary polydipsia

A

Is characterised by excessive fluid intake in the absence of physiological stimuli to drink

  • Driven by primary stimulation of the thirst centre in the hypothalamus
23
Q

What is diabetes insipidus

A

Diabetes insipidus (DI) is caused by a problem with either the production, or action, of the hormone vasopressin (AVP).

If you have DI your kidneys are unable to retain water. This leads to the production of large volumes of urine and, in turn, greatly increased thirst

24
Q

What can cause diabetes insipidus

A
  • Lack of vasopressin production by the pituitary
25
Q

What is nephrogenic diabetes insipidus

A
  • Nephrogenic diabetes insipidus (also known as renal diabetes insipidus) is a form of diabetes insipidus primarily due to pathology of the kidney (kidney is resistant to vasopressin)
  • This is in contrast to central/neurogenic diabetes insipidus, which is caused by insufficient levels of antidiuretic hormone
26
Q

Percentage of cases of cranial diabetes insipidus that are idiopathic and genetic

A
  • Idiopathic - 27%

- Genetic - <5%

27
Q

Genes implicated in cranial diabetes insipidus

A
  • Familial (AD) mutation of AVP gene
28
Q

Secondary causes of cranial diabetes insipidus

A

• Post-surgical (pituitary / other brain operations)
• Traumatic (head injury, including closed injury)
• Rarer causes
○ Tumours, histiocytosis, sarcoidosis, encephalitis, meningitis, vascular insults, autoimmune

29
Q

What is polyuria

A
  • Excessive or an abnormally large production or passage of urine (greater than 2.5 or 3 L over 24 hours in adults).
  • Frequent urination is usually an accompanying symptom
30
Q

Features of hypothalamic syndrome

A
  • Disordered thirst and DI
  • Disordered appetite (hyperphagia)
  • Disordered temperature regulation
  • Disordered sleep rhythm
  • Hypopituitarism
31
Q

Genes implicated in nephrogenic diabetes insipidus

A
  • Genetic (rare) Xr or Ar

- Mutations of V2 receptor gene/aquaporin gene

32
Q

Cranial vs nephrogenic diabetes insipidus

A

cranial diabetes insipidus – where the body doesn’t produce enough AVP, so excessive amounts of water are lost in large amounts of urine

nephrogenic diabetes insipidus – where AVP is produced at the right levels but, for a variety of reasons, the kidneys don’t respond to it in the normal way

33
Q

Most common cause of acquired nephrogenic diabetes insipidus

A
  • Lithium
34
Q

What is the water deprivation test

A
  • Period of dehydration
  • Measure plasma and urine osmolalities and weight
  • Injection of synthetic vasopressin - desmopressin
  • Measure plasma and urine osmolalities
35
Q

Normal response to water deprivation test

A
  • Normal plasma osmolality, high urine osmolality
36
Q

Water deprivation test response - cranial diabetes insipidus

A
  • Poor urine concentration after dehydration

- Rise in urine osmolality after desmopressin

37
Q

Water deprivation test response - nephrogenic diabetes insipidus

A
  • Poor urine concentration after dehydration

- No rise in urine osmolality after desmopressin

38
Q

Treatment - cranial diabetes insipidus

A
  • DDAVP (desmopressin)

- Over-treatment can cause hyponatraemia

39
Q

Treatment - nephrogenic diabetes insipidus

A
  • Correction of cause (metabolic/drug cause)

- Thiazide diuretics/NSAIDs

40
Q

Treatment - primary polydipsia

A
  • Explanation, persuasion

- Psychological therapy

41
Q

Hyponatraemia - definitions

A
  • [Sodium] < 135 mmol/L

- Severe [Na] <125 mmol/L

42
Q

Symptoms of hyponatraemia

A
  • May be asymptomatic
  • Depends on rate of fall as well as absolute value (brain adapts - chronic)
  • Non-specific - headache, nausea, mood change, cramps, lethargy
  • Severe/sudden - confusion, drowsiness, seizures, coma
43
Q

What do you exclude when classifying hyponatraemia

A
  • Exclude ‘drug’ causes
    • Thiazide diuretics, others
  • Exclude high concentrations of
    • Glucose, plasma lipids or proteins
44
Q

Classifying hyponatraemia by extracellular fluid volume status

A

• Hypovolaemia
- Renal loss, non-renal loss (D&V, burns, sweating)

• Normovolaemia (euvolaemia)

  • Hypoadrenalism, hypothyroidism
  • Syndrome of inappropriate ADH secretion (SIADH)

• Hypervolaemia
- Renal failure, cardiac failure, cirrhosis, excess IV dextrose

45
Q

What is SIADH

A

The syndrome of inappropriate antidiuretic hormone secretion (SIADH) is defined by the hyponatremia and hypo-osmolality resulting from inappropriate, continued secretion or action of the antidiuretic hormone arginine vasopressin (AVP) despite normal or increased plasma volume, which results in impaired water excretion

46
Q

SIADH - diagnosis

A

• Clinically euvolaemic patient
• Low plasma sodium and low plasma osmolality
Inappropriately high urine sodium concentration and high urine osmolality

47
Q

Assessment - SIADH

A

Assess renal, adrenal and thyroid function

48
Q

Causes of SIADH

A
  • Neoplasias, neurological disorders (CNS), lung disease, drugs, endocrine (hypothyroid/hypoadrenalism)
49
Q

SIADH treatment

A
  • Identify and treat the underlying cause
  • Fluid restriction (<1000 ml daily)
    • Induce negative fluid balance 500 ml
    • Aim ‘low normal’ sodium
  • Demeclocycline
    • Drug that induces mild nephrogenic DI
  • Vasopressin (V2 receptor) antagonists
    • “Vaptans” – induce a water diuresis
    • Expensive, variable responses, some attenuation
    • Lack of clinically significant outcome data
50
Q

Hyponatraemia treatment

A
  • Correct severe hyponatraemia slowly
  • Rapid correction risks oligodendrocyte degeneration and CNS myelinolysis (osmotic demyelination)
    • Severe neurological sequelae, may be permanent
    • Alcoholics & malnourished particularly at risk

Year 2 - T2 Theme 1 (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions