Regulation of ECF Volume and Osmolality

Question 1

What two components make up ECF?

Answer 1

Interstitial fluid
Transcellular fluid
Plasma

Question 2

What happens when the ECF osmolarity is hypertonic?

Answer 2

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

Question 3

What is an isotonic solution?

Answer 3

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

Question 4

How do disturbances in serum osmolality come about?

Answer 4

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

Question 5

What happens when there is a disturbance in serum osmolality?

Answer 5

Compensatory mechanisms increase total body water

Question 6

How do disturbances in volume come about?

Answer 6

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

Question 7

What happens when there are disturbances in volume?

Answer 7

Compensatory mechanisms increase body water and electrolytes

Question 8

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

Answer 8

Receptors sense high osmolality and causes:

Thirst causes increased water intake = dilute ECF

Increased ADH secretion = water retention = dilute ECF

Question 9

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

Answer 9

Increased plasma osmolality
Sensed by osmoreceptors in anterior hypothalamus

Decreased plasma volume/low blood pressure
Stimulates baroreceptors

Question 10

Where is ADH synthesized and stored?

Answer 10

Synthesized in hypothalamus
Stored in posterior pituitary

Question 11

What is found in anterior pituitary?

Answer 11

Osmoreceptors

Question 12

What factors cause ADH secretion to decrease?

Answer 12

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

Question 13

What factors cause ADH secretion to increase?

Answer 13

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

Increased plasma osmolality
Decreased ECF and low blood pressure

Question 14

What happens to a person with no access to water?

Answer 14

Increased ECF osmolality and decreased ECF volume
SO increased ADH levels

Question 15

What happens when ADH binds V1 receptor?

Answer 15

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

Question 16

What happens when ADH binds V2 receptor?

Answer 16

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

Question 17

Where is V2 receptor located?

Answer 17

Late distal tubules and collecting duct

Question 18

When urine is dilute, what is the osmolality?

Answer 18

Low osmolality ~50

Question 19

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

Answer 19

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

Question 20

What are the consequences of SIADH?

Answer 20

Water retention = leading to swelling
Low Na+ levels

Question 21

What does failure of producing ADH cause?

Answer 21

Central diabetes insipidus

Question 22

What does inability of kidneys to respond to ADH cause?

Answer 22

Nephrogenic diabetes indipidus

Question 23

What are the consequences of diabetes insipidus?

Answer 23

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

Question 24

Howa re central and nephrogenic diabetes insipidus distinguished?

Answer 24

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

Question 25

What happens when you are thirsty?

Answer 25

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

Question 26

What happens to restore ECF volume when it is reduced?

Answer 26

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

Question 27

Why reduce ANP when ECF volume is low?

Answer 27

Normally, ANP promotes water and Na+ excretion and causes vasodilation So reducing ANP will reasborb water and Na+

Question 28

What is renin and where is it secreted?

Answer 28

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

Question 29

Where are catecholamines secreted?

Answer 29

Adrenal medulla

Question 30

Name the steps of RAAS

Answer 30

Kidney secretes renin enzyme Liver secretes angiotensinogen Angiotensinogen -> Ang I by renin Ang I >> 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

Question 31

What two factors increase aldosterone?

Answer 31

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

Question 32

Where is aldosterone made and released?

Answer 32

Zone glomerulosa of ADRENAL cortex

Question 33

What are the effects of aldosterone?

Answer 33

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+

Question 34

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

Answer 34

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.

Question 35

What are NSAIDS function?

Answer 35

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

Question 36

What is the role of prostaglandins?

Answer 36

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

Question 37

What is Ealkiren?

Answer 37

Renin inhibitor

Question 38

What are natriuretic peptides released by?

Answer 38

Cardiac muscle fibres

Question 39

What triggers natriuretic peptides release?

Answer 39

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

Question 40

What are the effects of ANP?

Answer 40

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

Question 41

What factors stimulate renin secretion?

Answer 41

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

Question 42

What factors inhibit renin secretion?

Answer 42

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