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Advanced Physiology > Fluid & Electrolyte Homeostasis > Flashcards

Fluid & Electrolyte Homeostasis Flashcards

1
Q

What percentage of total body weight does fluid make up?

A

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

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2
Q

What percentage of extracellular fluid is interstitial fluid?

A

80%

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3
Q

What type of tissue contains the least amount of fluid?

A

Adipose tissue

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4
Q

Why are salts important?

A
  • Neuromuscular excitability - Secretory activity - Membrane permeability - Controlling fluid movements
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5
Q

What are two qualities of electrolytes?

A

They dissociate in water & are electrically charged

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6
Q

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?

A

Sodium salts; 280mOsm

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7
Q

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

A
  • Sodium is the only cation to exert significant osmotic pressure - Sodium ions being leaked into cells/pumped out against their electrochemical gradient
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8
Q

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

A

True

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9
Q

What do changes in plasma sodium levels affect?

A

Plasma volume/blood pressure & ICF/interstitial fluid volumes

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10
Q

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

A

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

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11
Q

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

A

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

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12
Q

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

A

Linear

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13
Q

What is specific gravity?

A

A measure of the weight of solutes in urine

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14
Q

What is specific gravity influenced by and why?

A

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

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15
Q

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

A

They both remain relatively stable

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16
Q

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

A

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

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17
Q

What is diuresis?

A

An increase in urine output

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18
Q

How is a dilute urine formed?

A

Continue electrolyte reabsorption, decrease water reabsorption

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19
Q

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

A

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

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20
Q

How is a concentrated urine formed?

A

Continue electrolyte reabsorption, increase water reabsorption

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21
Q

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

A

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

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22
Q

What is obligatory urine volume and what is the formula?

A

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

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23
Q

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

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

A

b) increased obligatory urine volume

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24
Q

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

A

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*

25
Q

Where is ADH synthesised, released and actioned?

A

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

26
Q

What are the stimuli for ADH secretion?

A

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

27
Q

Is plasma osmolarity or blood volume more sensitive to change?

A

Plasma osmolarity

28
Q

What are the stimuli for decreased ADH secretion?

A

Decreased osmolarity, increased blood pressure/volume, alcohol

29
Q

What are the stimuli for thirst?

A

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

30
Q

What is angiotensin II?

A

The body’s most potent vasoconstrictor

31
Q

What are the stimuli for decreased thirst?

A

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

32
Q

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

A

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

33
Q

What is the renal-body fluid feedback system?

A

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

34
Q

Where is aldosterone produced?

A

Adrenal cortex

35
Q

How does aldosterone regulate sodium balance?

A
  • Sodium reabsorption (65% in proximal tubules, 25% in loop of Henle)
  • When aldosterone levels are high, remaining sodium is actively reabsorbed from filtrate
36
Q

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

A

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

37
Q

How does the renin-angiotensin mechanism trigger aldosterone release?

A
  • 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
38
Q

How does aldosterone increase ECF sodium levels?

A

Increased water reabsorption, reduced urine output, increased blood volume

39
Q

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

A

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

40
Q

What is pressure diuresis and what does it do?

A

The baroreceptor-renal system mechanism, decreases blood pressure

41
Q

What happens when systemic blood pressure decreases?

A

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

42
Q

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

A

By inhibiting sodium/water retention and events that promote vasoconstriction

43
Q

What does ANP target in order to reduce blood pressure?

A

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

44
Q

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

A

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

45
Q

What are the consequences of hyperkalemia and hypokalemia?

A

Diruption of electrical conduction in the heart and sudden death

46
Q

Where and how is potassium balance controlled?

A

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

47
Q

What happens when ECF potassium levels are high?

A

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

48
Q

What effect does aldosterone have on potassium balance?

A

Stimulates potassium secretion by the principal cells

49
Q

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

A

1:1

50
Q

How does potassium control its own ECF concentration?

A

By negative feedback regulation of aldosterone release

51
Q

What is ionic calcium in ECF important for?

A

Blood clotting, cell membrane permeability, secretory behaviour

52
Q

What does hypocalcemia cause?

A

Increased excitability of muscles & muscle tetany (cramps)

53
Q

What does hypercalcemia cause?

A

Inhibitionn of neurons and muscle cells and heart arrhythmias

54
Q

What hormones control calcium balance?

A

Parathyroid hormone and calcitonin

55
Q

How does PTH promote increases in calcium levels?

A

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

56
Q

What does calcium reabsorption go hand in hand with?

A

Phosphate excretion

57
Q

Where is filtered phosphate actively reabsorbed?

A

Proximal tubules

58
Q

What happens when ECF calcium levels are normal or high?

A

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

Advanced Physiology (10 decks)

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