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Human Physiology Y3 > Regulation of ECF Volume and Osmolality > Flashcards

Regulation of ECF Volume and Osmolality Flashcards

1
Q

What two components make up ECF?

A

Interstitial fluid
Transcellular fluid
Plasma

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2
Q

What happens when the ECF osmolarity is hypertonic?

A

This is when ECF has more solutes compared to ICF
Water leaves the cells to more into the ECF
Cells shrink

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3
Q

What is an isotonic solution?

A

A solution with the same osmolality as a cell = same number of osmotically active particles

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4
Q

How do disturbances in serum osmolality come about?

A

Pure water loss without losing electrolytes = not drinking water
ECF osmolality increases and volume reduces

Increase osmotically active external substances = high blood sugar, ingestion of toxins
ECF osmolality increase but volume is normal

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5
Q

What happens when there is a disturbance in serum osmolality?

A

Compensatory mechanisms increase total body water

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6
Q

How do disturbances in volume come about?

A

Fluid and electrolytes lost = vomiting and dearrhea
ECF volume is reduced but osmolality is normal

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7
Q

What happens when there are disturbances in volume?

A

Compensatory mechanisms increase body water and electrolytes

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8
Q

What compensatory mechanisms occur when there is an increased ECF osmolality?

A

Receptors sense high osmolality and causes:

Thirst causes increased water intake = dilute ECF

Increased ADH secretion = water retention = dilute ECF

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9
Q

What are the two reasons ADH synthesis and release is increased?

A

Increased plasma osmolality
Sensed by osmoreceptors in anterior hypothalamus

Decreased plasma volume/low blood pressure
Stimulates baroreceptors

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10
Q

Where is ADH synthesized and stored?

A

Synthesized in hypothalamus
Stored in posterior pituitary

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11
Q

What is found in anterior pituitary?

A

Osmoreceptors

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12
Q

What factors cause ADH secretion to decrease?

A

Alcohol
Increased ECF and blood pressure
Reduced plasma osmolality = less solutes to the volume so decrease the volume

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13
Q

What factors cause ADH secretion to increase?

A

Pain, emotion, stress, nausea, vomiting and Angiotensin II

Increased plasma osmolality
Decreased ECF and low blood pressure

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14
Q

What happens to a person with no access to water?

A

Increased ECF osmolality and decreased ECF volume
SO increased ADH levels

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15
Q

What happens when ADH binds V1 receptor?

A

Vasoconstriction = acts at V1 in vascular smooth muscle
Water reabsorption and concentration of urine = acting at V2 receptors
Increases reabsorption of urea at medullary

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16
Q

What happens when ADH binds V2 receptor?

A

Stimulates movement of AQP2 to luminal side of cell
AQP2 forms water channel = permitting rapid diffusion of water through the cells
Increases water absorption
Reduces urinary volume and increases urine osmolality

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17
Q

Where is V2 receptor located?

A

Late distal tubules and collecting duct

18
Q

When urine is dilute, what is the osmolality?

A

Low osmolality ~50

19
Q

What does SIADH stand for and how does it come about?

A

Syndrome of inappropriate antidiuretic hormone ADH release (SIADH)

A case of antidiuretic hormone (ADH) from the pituitary gland or non-pituitary sources or its continued action on vasopressin receptors

20
Q

What are the consequences of SIADH?

A

Water retention = leading to swelling
Low Na+ levels

21
Q

What does failure of producing ADH cause?

A

Central diabetes insipidus

22
Q

What does inability of kidneys to respond to ADH cause?

A

Nephrogenic diabetes indipidus

23
Q

What are the consequences of diabetes insipidus?

A

ADH deficiency or inability to respond to it = inability to concentrate urine

Production of large amount of dilute urine = polyuria

Dehydration leading to increased thirst = 1
polydipsia

Increased water intake

24
Q

Howa re central and nephrogenic diabetes insipidus distinguished?

A

Administration of desmopressin = analogue of ADH
Urine output will reduce in central DI because can still respond to the analogue

25
Q

What happens when you are thirsty?

A

Dry mouth
Increased plasma osmolarity
Increased angiotensin II = to vasoconstrict and counter balance blood pressure
Decreased blood volume and pressure = because less fluid

26
Q

What happens to restore ECF volume when it is reduced?

A

Reduced ANP
Increased ADH < due to increased sympathetic activity and activation of RAAS
RAAS activates thirst mechanism

27
Q

Why reduce ANP when ECF volume is low?

A

Normally, ANP promotes water and Na+ excretion and causes vasodilation

So reducing ANP will reasborb water and Na+

28
Q

What is renin and where is it secreted?

A

Acid protease secreted to the blood stream
Secreted by granular cells in juxtaglomerula apparatus

29
Q

Where are catecholamines secreted?

A

Adrenal medulla

30
Q

Name the steps of RAAS

A

Kidney secretes renin enzyme
Liver secretes angiotensinogen
Angiotensinogen -> Ang I by renin
Ang I&raquo_space; Ang II by ACE in endothelium

AngII causes vasoconstriction in cardiovascular system
AngII stimulates release of aldosterone from adrenal cortex (above kidney)
Both these effects increase blood pressure

31
Q

What two factors increase aldosterone?

A

Major factor = increased Ang II
Minor factor = increased extracellular K+ conc

32
Q

Where is aldosterone made and released?

A

Zone glomerulosa of ADRENAL cortex

33
Q

What are the effects of aldosterone?

A

Increases Na permeability of luminal side of membrane by insertion of EnaC

Stimulating Na+/K+ pump on basolateral side of PRINCIPAL cells of DCT and collecting tube

Both of these increases Na reabsorption and K+ secretion
Increasing ECF volume and reduce serum K+

34
Q

What is the role of beta blockers, and how do they achieve this?

A

Beta blockers reduce sympathetic effects by binding to beta-adrenergic receptors = where catecholamines usually bind

Reduce sympathetic stimulation of renin release, thereby attenuating the activation of the RAAS.

35
Q

What are NSAIDS function?

A

Reduce prostaglandins

This causes vasoconstriction of the afferent arteriole = leading to decreased renal blood flow and GFR

36
Q

What is the role of prostaglandins?

A

Modulating renal blood flow and glomerular filtration rate (GFR) by dilating the renal vasculature and promoting vasodilation of the afferent arteriole.

37
Q

What is Ealkiren?

A

Renin inhibitor

38
Q

What are natriuretic peptides released by?

A

Cardiac muscle fibres

39
Q

What triggers natriuretic peptides release?

A

Produced in response to cardiac stretching or increased ECF/blood volume

40
Q

What are the effects of ANP?

A

ANP acts on the kidneys to promote sodium excretion (natriuresis) and water excretion (diuresis), leading to decreased blood volume and blood pressure.

Additionally, ANP inhibits the secretion of renin and aldosterone, which helps to counteract the effects of RAA) and promote vasodilation

41
Q

What factors stimulate renin secretion?

A

Increasing sympathetic activity via renal nerves
Increased circulating catecholamines
Low ECF volume = due to bleeding, dehydration, diuretics
Prostaglandins

42
Q

What factors inhibit renin secretion?

A

Increased Na and Cl absorption from macula densa
Increased afferent arteriolar pressure
Angiotensin II = product inhibition
Vassopressin

Human Physiology Y3 (14 decks)

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