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203 [1] - Endocrine System > L10 - Physiology of Thirst and Fluid Balance and its Disorders > Flashcards

L10 - Physiology of Thirst and Fluid Balance and its Disorders Flashcards

1
Q

what is the importance of water homeostasis

what are the 3 key determinants

A

Importance:
• Regulation of water balance ensures plasma osmolality (and extracellular fluid osmolality) remains stable

Narrow range of plasma
osmolality
— 285-295 mosmol/kg

3 key determinants:

Antidiuretic hormone (ADH)
— Osmotically stimulated
secretion
— Acts on renal tubule to allow changes in water excretion

Kidney
Wide variation in urine
output (0.5-20 L/day)

Thirst
— Osmoregulated
— Stimulates fluid intake output (0 5 -20 /day )

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2
Q

Osmoreceptors

what are they

where are they located

what do they do

what does this initiate

A

• Osmoreceptors are groups of specialised cells which detect changes in plasma osmolality (esp sodium)

• Located in the anterior wall of 3rd ventricle
— Fenestrations in the blood-brain barrier allow circulating solutes (osmoles) to influence brain osmoreceptors

’ 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

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3
Q

What is ADH

what is the human form

how is it similar to oxytocin (properties wise)

A 
Anti-diuretic hormone (ADH) 
ADH = 'against a 
diuresis' — water 
conserving 
' Human form of ADH is 
arginine vasopressin 
(AVP) 
' Like oxytocin: 
— Nonapeptide -9 amino 
acid peptide 
— Vasopressin synthesised 
in neurons in supraoptic and paraventricular nuclei of the hypothalamus 
— Secretory granules 
migrate down axons to 
posterior pituitary from 
where AVP is released 
( AVP )
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4
Q

ADH action in the kidney

what is it mediated by

what happens after this

what happens after ADH is cleared

A

ADH action mediated via V2 receptors
‘ ADH-sensitive water channel (aquaporin) normally stored in cytoplasmic vesicles, moves to & fuses with the luminal membrane

’ 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

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5
Q

OSMOREGULATION

what happens with AVP and kidney at high and low plasma osmolality

what happens with thirst at low and high

A

AVP and the kidney—

• Low plasma osmolality 
— AVP undetectable 
— Dilute urine 
High urine output 
High plasma osmolality

High AVP secretion
— Concentrated urine
Low urine output

Thirst—-

’ Low plasma osmolality
— No thirst

High osmolality 
— Increased thirst sensation 
— Drinking immediately 
transiently suppresses AVP secretion and thirst 
• Avoids 'overshoot' 
Low plasma osmolality
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6
Q

what is the relationship between plasma AVP and plasma / urine osmolality

A

increases

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7
Q

POLYURIA AND POLYDIPSIA

what do you want to exclude

what are the 3 other main causes

A

Exclude diabetes mellitus

— 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’

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8
Q

CRANIAL DIABETES INSIPIDUS

what are the various causes of it?

A

’ Idiopathic (27%)

Genetic (<5%)
— Familial (AD) mutation of AVP gene
— DIDMOAD (Wolfram) (Ar, incomplete penetrance)

’ Secondary (commonest causes)—–

— Post-surgical (pituitary / other brain operations)

— Traumatic (head injury, including closed injury)

— Rarer causes
• Tumours, histiocytosis, sarcoidosis, encephalitis, meningitis, vascular insults, autoimmune

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9
Q

CRANIAL DI

what causes it
what happens with it
what can help keep a stable plasma osmolality

A

Decreased osmoregulated AVP secretion

’ Excess solute-free renal water excretion
— polyuria

’ Provided thirst sensation remains intact and there is ready access to fluids, thirst is stimulated to maintain a stable, normal plasma osmolality
— polydipsia

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10
Q

Hypothalamic syndrome

what is it
what the effects of it

A 
Disordered thirst and DI 
Disordered appetite 
(hyperphagia) 
Disordered temperature 
regulation 
Disordered sleep rhythm 
Hypopituitarism
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11
Q

NEPHROGENIC DIABETES INSIPIDUS

what happens here

A

’ Renal tubules resistant to AVP
— Polyuria

’ Thirst stimulated
— Polydipsia

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12
Q

NEPHROGENIC DIABETES INSIPIDUS

what are the various causes

A

’ Idiopathic

Genetic (rare) Xr or Ar
— Mutations of V2 receptor gene / aquaporin gene

’ Metabolic
— High [calcium] or low [potassium]

’ Drugs
— Lithium

’ Chronic kidney disease

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13
Q

what is primary polydipsia

what happens with it

what are the various effects

A

’ Increased fluid intake
— polydipsia

’ Lower plasma osmolality

’ Suppressed AVP secretion

’ Low urine osmolality, high urine output
— Polyuria

Also lose renal interstitial solute, reducing renal concentrating ability

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14
Q

Investigating polyuria and polydipsia

what would you do and what would u exclude and what would you document and tests

A

’ Medical History

Exclude diabetes mellitus

’ Document 24 hour fluid balance
— Urine output and fluid intake, day & night

’ Exclude hypercalcaemia / hypokalaemia

’ Water deprivation test

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15
Q

Water deprivation test

what happens
what is done what is measured what is given

A

’ Period of dehydration

’ Measure plasma and urine osmolalities & weight

’ Injection of synthetic vasopressin
- Desmopressin (DDAVP)

’ Measure plasma and urine osmolalities

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16
Q

water deprivation test

what is a normal response to dehydration?

what would happen with crainial and nephrogenic DI to urine osmolality / conc after dehydration or desmopressin

A

Normal response to dehydration
— Normal plasma osmolality, high urine osmolality

’ Cranial diabetes insipidus
— Poor urine concentration after dehydration
— Rise in urine osmolality after desmopressin

’ Nephrogenic diabetes insipidus
— Poor urine concentration after dehydration
— No rise in urine osmolality after desmopressin

17
Q

what is the treatment for cranial DI, nephrogenic DI and primary polydipsia

(what happens with overtreatment of cranial DI)

A

’ Cranial diabetes insipidus
— DDAVP (desmopressin)
— Over-treatment can cause hyponatraemia

’ Nephrogenic diabetes insipidus
— Correction of cause (metabolic / drug cause)
— Thiazide diuretics / NSAlDs

’ Primary polydipsia
— Explanation, persuasion
— Psychological therapy

18
Q

HYPONATRAEMIA

what is the definition? severe?

what are the symptoms

A

[Sodium] <135 mmol/L
Severe [Na] <125 mmol/L

SYMP
–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

19
Q

CLASSIFYING OF HYPONATRAEMIA

what would you exclude in terms of causes
what would you exclude in terms of high concs

how DO you classify? (3 types)
—causes for each?

A

Exclude ‘drug’ causes
— Thiazide diuretics, others
Exclude high concentrations of
— Glucose, plasma lipids or proteins

’ Classify by extracellular fluid volume status

— 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

20
Q

SIADH

what signs would help diagnose the patent

what would you assess

what are some causes of SIADH

A

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

’ Assess renal, adrenal and thyroid function

Many causes
— Neoplasias, neurological disorders (CNS), lung disease,
drugs, endocrine (hypothyroid/hypoadrenalism)

21
Q

SIADH treatment

what are the options what do each of these do

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

22
Q

Hyponatraemia treatment

why is it important to correct severe hyponatraemia a certain way

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

203 [1] - Endocrine System (23 decks)

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