5 Water Balance Flashcards
Q: What is osmolarity? to do with? Depends on?
A: measure of the solute concentration in a solution (osmoles/liter; 1 Osmole = 1 mole of dissolved solutes per liter)
to do with number of particles
depends on the number of dissolved solutes present (The greater the number of dissolved particles, the greater the osmolarity)
Q: Compare plasma and urine osmolarity.
A: plasma = homeostatic set point = maintained at 285/295 mOsmol/L
urine= wide range from hypoosmolar (lower particle content) to hyperosmolar (depends on conditions)
Q: How does water move in terms of osmolarity?
A: Water flows across a semi permeable membrane from a region of low osmolarity to a region of high osmolarity
Q: How can osmolarity be increased? Decreased? What kind of system is this?
A: increased salt
decreased salt
variable osmolarity system that we don’t have
Q: What kind of osmolarity system do we operate under? When do we increase volume? Decrease volume?
A: constant osmolarity
increased salt (would need to increase water to maintain osmolarity)
decreased salt (would need to decrease water to maintain osmolarity)
Q: On average, how does the water we consume compare to water and salt we need to replace? Therefore we must get rid of? (3)
A: On an average day we consume 20-25% more water and salt than we need to replace that lost
- Must get rid of the excess volume (or we will expand)
- Must get rid of any excess water (To keep osmolarity up, or we will expand)
- Must get rid of any excess salt (to stop osmolarity going too high)
Q: What’s the most abundant component of plasma? Most prevalent solute? figure? Where are these 2 answers also correct?
A: water
Na, around 140mmol/L out of 285-295mmol/L
ECF
Q: Why do we balance water? Why do we regulate salt levels?
A: to regulate plasma osmolarity
determine ECF volume
Q: How is our total body water content split? (5) How many litres do we roughly contain?
A: total= around 40L
65% = intracellular fluid compartment (35L)
35% = extracellular compartment (15L)
- interstitual
- plasma
- lymph
- transcellular (cerebrospinal fluid etc)
Q: What’s the main content difference between intracellular fluid and extracellular? (2) 2 examples of extracellular fluid? Main differnece?
A: more phosphate in cells, more chloride outside of cells
more protein in plasma than interstitual fluid
Q: How do we get rid of water and how does each method vary? (4) How much is lost on average via each method?
A: Skin and sweat: variable but uncontrollable
Normally about 450 mls/day - changes with fever, climate and activity
Faeces: uncontrollable
normally about 100 ml/day - Diarrhoea up to 20L/day with cholera
Respiration: uncontrollable
350mls/day - changes with activity
Urine output: variable and controllable
1500 mls/day - largest component
Q: Outline water movement in a nephron. (5) Where does regulation occur? concentration effects also occur where?
A: -lots absorbed in proximal tubule- 30% of input remains
- some movement in descending LoH
- none in ascending LoH
- some in distal CT- left with 20% of input
- water movement in collecting tubule- left with <1% to 10% of the original input
collecting duct, LoH
Q: How does medulla size relate to urine concentration? Example?
A: size affects conc
kangaroos have large medulla to cortical ratio
Q: How does water move? Problem? Solution? How does this present itself in real life?
A: by osmosis
can’t pump
produce region of hyperosmolar interstitual fluid
-as a gradient from cortex->outer medulla->inner medulla (low osmolarity->high)
Q: Osmolarity gradient from cortex to outer to inner medulla. What are the 4 components involved?
A: 1. countercurrent between desc and asc limb- as water comes done desc, water will leave
- cells of desc limb don’t do significant amount of active transport- don’t have many mitochondria but are permeable to water as tight junctions are not that tight
- bottom of LoH is permeable to urea
- thick asc limb has high number of mito and active transport capacity- include triple transport pump of Na, K and Cl entering
Q: Osmolarity gradient from cortex to outer to inner medulla. How is it established? (7)
A: UNIFORM POSITION
- gradient at top of asc limb= made 200mmol/L across membrane (all way down) by pumping Na and Cl out of cells
- descending limb re equibrilates as a result by water moving out -> have 400mmol/L in middle
- tubular fluid enters (around 300mmol/L) and you get some movement of water from tubules to outside until similar osmolarity
- asc limb is still pumped salt out to give gradient across wall -> make 200mmol/L at top of asc limb, then get 350mmol/L just below
- REPEAT -> can generate much higher concentration lower down asc limb -> 500mmol/L
- -> get 600mmol/L at bottom then slightly higher concentration than normal at tpop = 305mmol/L
- keep getting higher osmolarity at lower parts of asc limb than high parts of asc limb
GRADIENT ONCE ESTABLISHED
Q: What parts of the nephron are permeable to urea? (2)
A: lower part of collecting duct and tip of LoH
Q: Describe the loop movement of urea. (5)
A: 1. water leaves desc limb of LoH but urea does not = increases concentration of urea in tube
- as more water leaves the top of the collecting duct= urea concentration increases even more
- urea concentration is high enough to move out of tubeles
- concentration of urea is higher in medulla than tip of LoH
- movement of urea back into LoH tip
Q: Name 4 urea channels are list where they are.
A: UT-A1 and 3 are in collecting duct
UT-A2 in descending limb
UT-B1 in descending vasa recta (series of straight capillaries in the medulla that lie parallel to the loop of Henle)
Q: What happens when there are a lack of UT-A1 and 3 receptors in mice? (4)
A: reduced urea in medulla (less urea can move from CD to it)
severe reduction in ability to concentrate urine
increased water intake by 20%
no ability to reduce urine output if water restricted for 24h
Q: What happens when there are a lack of UT-A2 receptors in mice? When are the effects observed?
A: very mild phenotype
only observed on low protein diet (less protein and nitrogen)
Q: What happens when there are a lack of UT-B receptors in mice? (3)
A: increased urine production
reduced urine concentrating ability
weight loss
Q: Describe problems in urea transporters in humans. (3)
A: no UT A1 or 3 mutations have been seen
Point mutations in UT-A2 have been observed: Reduced blood pressure (getting rid of more water)
Loss of function mutations in UT-B are observed: Reduction in urine concentrating ability
Q: What determines a species ability to create a urine osmolarity?
A: Na/K ATPase activity (not size/length of LoH)
