Fluid & Electrolyte Homeostasis

Question 1

What percentage of total body weight does fluid make up?

Answer 1

60% - 40% intracellular fluid and 20% extracellular fluid

Question 2

What percentage of extracellular fluid is interstitial fluid?

Answer 2

80%

Question 3

What type of tissue contains the least amount of fluid?

Answer 3

Adipose tissue

Question 4

Why are salts important?

Answer 4

• Neuromuscular excitability - Secretory activity - Membrane permeability - Controlling fluid movements

Question 5

What are two qualities of electrolytes?

Answer 5

They dissociate in water & are electrically charged

Question 6

What type of salts account for 90-95% of all solutes in the ECF and how many mOsm do they contribute to the total 300mOsm ECF solute concentration?

Answer 6

Sodium salts; 280mOsm

Question 7

Why does sodium play a role in controlling ECF volume and water distribution in the body?

Answer 7

• Sodium is the only cation to exert significant osmotic pressure - Sodium ions being leaked into cells/pumped out against their electrochemical gradient

Question 8

True or false: Sodium concentration in the ECF normally remains stable

Answer 8

True

Question 9

What do changes in plasma sodium levels affect?

Answer 9

Plasma volume/blood pressure & ICF/interstitial fluid volumes

Question 10

What is the meaning of ‘renal acid-base control mechanisms are coupled to sodium ion transport’?

Answer 10

H+ and Na+ are swapped - where sodium goes, water actively follows

Question 11

What are the normal and maximal (dehydrated) urine concentrations?

Answer 11

Normal: 50-70 mOsm/L Maximal: 1200-1400 mOsm/L

Question 12

What type of relationship exists between urine osmolarity and urine specific gravity?

Answer 12

Linear

Question 13

What is specific gravity?

Answer 13

A measure of the weight of solutes in urine

Question 14

What is specific gravity influenced by and why?

Answer 14

Glucose & protein in urine - not normal constituents of urine (increased solutes = increased weight = increased SG)

Question 15

What happens to urinary solute excretion and plasma osmolarity following ingestion of 1L of water?

Answer 15

They both remain relatively stable

Question 16

What happens to urine flow and urine osmolarity following ingestion of 1L of water?

Answer 16

Urine flow: Sharp increase, plateau, sharp decrease Urine osmolarity: Sharp decrease (more diluted), plateau, sharp increase

Question 17

What is diuresis?

Answer 17

An increase in urine output

Question 18

How is a dilute urine formed?

Answer 18

Continue electrolyte reabsorption, decrease water reabsorption

Question 19

What is the mechanism behind the formation of a dilute urine?

Answer 19

Decreased ADH release (no aquaporins formed = more water in filtrate) & water permeability in distal/collecting tubules

Question 20

How is a concentrated urine formed?

Answer 20

Continue electrolyte reabsorption, increase water reabsorption

Question 21

What is the mechanism behind the formation of a concentrated urine?

Answer 21

Increased ADH release increases water permeability in distal/collecting tubules (opens aquaporins & allows water to leak out), high osmolarity of renal medulla, countercurrent flow of tubular fluid

Question 22

What is obligatory urine volume and what is the formula?

Answer 22

The minimum urine volume in which the excreted solute can be dissolved and excreted

Amount of solute that must be excreted each day to maintain electrolyte balance/Max urine osmolarity

i.e. 600mOsm/d / 1200mOsm/L = 0.5L/day

Question 23

During renal disease, urine concentrating ability is impaired, resulting in

a) decreased obligatory urine volume
b) increased obligatory urine volume

Answer 23

b) increased obligatory urine volume

Question 24

What is the osmoreceptor-ADH feedback mechanism for regulating extracellur fluid osmolarity?

Answer 24

Water deficit

= increased osmolarity

= increased ADH secretion

= increased plasma ADH

= increased H2O permeability in distal/collecting tubules

= decreased H2O excreted

*negative feedback to water deficit*

Question 25

Where is ADH synthesised, released and actioned?

Answer 25

Synthesised in the magnocellular neurons of the hypothalamus, released by the posterior pituitary, actioned on the kidneys

Question 26

What are the stimuli for ADH secretion?

Answer 26

Increased osmolarity, decreased blood pressure/volume, input from cerebral cortex (e.g. fear), nausea, angiotensin II, nicotine, morphine

Question 27

Is plasma osmolarity or blood volume more sensitive to change?

Answer 27

Plasma osmolarity

Question 28

What are the stimuli for decreased ADH secretion?

Answer 28

Decreased osmolarity, increased blood pressure/volume, alcohol

Question 29

What are the stimuli for thirst?

Answer 29

Increased osmolarity, decreased blood pressure/volume, increased angiotensin II, dryness of mouth

Question 30

What is angiotensin II?

Answer 30

The body's most potent vasoconstrictor

Question 31

What are the stimuli for decreased thirst?

Answer 31

Decreased osmolarity, increased blood pressure/volume, decreased angiotensin II, gastric distention

Question 32

When the ADH-thirst system is blocked and sodium is ingested, what happens to plasma sodium levels and why?

Answer 32

They dramatically increase, as the body is unable to counteract the change and control plasma sodium concentration

Question 33

What is the renal-body fluid feedback system?

Answer 33

Fluid intake = increased ECF volume = increased blood volume = increased mean circulatory filling pressure = increased venous return = increased cardiac output = increased total peripheral resistance = increased arterial pressure = dramatic increase in renal fluid excretion

Question 34

Where is aldosterone produced?

Answer 34

Adrenal cortex

Question 35

How does aldosterone regulate sodium balance?

Answer 35

- Sodium reabsorption (65% in proximal tubules, 25% in loop of Henle) - When aldosterone levels are high, remaining sodium is actively reabsorbed from filtrate

Question 36

What are the two triggers for the release of aldosterone to regulate sodium balance?

Answer 36

The renin-angiotensin mechanism & elevated potassium/decreased sodium levels in ECF

Question 37

How does the renin-angiotensin mechanism trigger aldosterone release?

Answer 37

- Juxtaglomerular apparatus releases renin in response to SNS stimulation, decreased filtrate osmolarity & decreased stretch - Renin catalyses production of angiotensin II - Angiotensin II stimulates aldosterone release

Question 38

How does aldosterone increase ECF sodium levels?

Answer 38

Increased water reabsorption, reduced urine output, increased blood volume

Question 39

What happens when baroreceptors alert the brain of increased blood volume/pressure?

Answer 39

SNS impulses to kidneys decline, afferent arterioles dilate, glomerular filtration rate increases, sodium & water output increases

Question 40

What is pressure diuresis and what does it do?

Answer 40

The baroreceptor-renal system mechanism, decreases blood pressure

Question 41

What happens when systemic blood pressure decreases?

Answer 41

Increased SNS impulses to the kidneys, afferent arterioles constrict, glomerular filtration rate decreases, sodium and water output decreases

Question 42

How does atrial natriuretic peptide (ANP) reduce blood pressure/volume?

Answer 42

By inhibiting sodium/water retention and events that promote vasoconstriction

Question 43

What does ANP target in order to reduce blood pressure?

Answer 43

JG apparatus of kidney (inhibits angiotensin II system), hypothalamus/posterior pituitary (decreased ADH release) & adrenal cortex (decreased aldosterone release)

Question 44

How does relative ICF-ECF potassium ion concentration affect a cell's resting membrane potential?

Answer 44

Excessive ECF potasisum decrease membrane potential, too little potassium causes hyperpolarisation

Question 45

What are the consequences of hyperkalemia and hypokalemia?

Answer 45

Diruption of electrical conduction in the heart and sudden death

Question 46

Where and how is potassium balance controlled?

Answer 46

In the collecting ducts of the cortex, by changing the amount of potassium secreted into filtrate

Question 47

What happens when ECF potassium levels are high?

Answer 47

Principal cells secrete potassium into filtrate for excretion, aldosterone is released

Question 48

What effect does aldosterone have on potassium balance?

Answer 48

Stimulates potassium secretion by the principal cells

Question 49

In the cortical collecting ducts, what is the ratio of sodium reabsorbed to potassium secreted?

Answer 49

1:1

Question 50

How does potassium control its own ECF concentration?

Answer 50

By negative feedback regulation of aldosterone release

Question 51

What is ionic calcium in ECF important for?

Answer 51

Blood clotting, cell membrane permeability, secretory behaviour

Question 52

What does hypocalcemia cause?

Answer 52

Increased excitability of muscles & muscle tetany (cramps)

Question 53

What does hypercalcemia cause?

Answer 53

Inhibitionn of neurons and muscle cells and heart arrhythmias

Question 54

What hormones control calcium balance?

Answer 54

Parathyroid hormone and calcitonin

Question 55

How does PTH promote increases in calcium levels?

Answer 55

By targeting bones (activates osteoclasts), small intestine (enhances absorption) & kidneys (enhances reabsorption/decreases phosphate reabsorption)

Question 56

What does calcium reabsorption go hand in hand with?

Answer 56

Phosphate excretion

Question 57

Where is filtered phosphate actively reabsorbed?

Answer 57

Proximal tubules

Question 58

What happens when ECF calcium levels are normal or high?

Answer 58

PTH secretion is inhibited, osteoclasts are inhibited, calcium is excreted & phosphate is reabsorbed