Regulation Of Urine Volume And Fluid Balance Flashcards
ACE inhibitors cause a marked reduction in renal function in patients with bilateral renal artery stenosis. Why?
W/o drug: Kidney will think BP is low due to narrowing even though it is normal -> RAAS will be activated producing angiotensin II
-> constricts the EA trying to increase BP = manages to maintain GFR
With drug: RAAS + angiotensin II is reduced -> EA will remain dilated = reducing GFR + renal function
How do the kidneys regulate fluid balance?
Regulate volume + composition by altering volume of plasma which in turn influences other fluid compartments (e.g. interstitial fluid)
Maintenance of volume linked to regulation of EC [Na] + [H2O] which in turn controls BP
What are the symptoms + signs of hypovolaemia?
Symptoms: thirst, dizziness on standing + confusion
Signs: low JVP, postural hypotension, weight loss, dry mucous membranes, reduced skin turgor + reduced urine output
What are the symptoms + signs of hypervolaemia?
Symptoms: ankle swelling + breathlessness
Signs: Raised JVP, oedema (peripheral +/- pulmonary), weight gain + hypertension
Why is it important to regulate osmolarity and how does the kidney do it?
To avoid excessive movements between compartments and subsequent cell dehydration or swelling
Control of osmolarity + volume linked to kidneys ability to alter urine volume/composition in response to wide range of fluid inputs/outputs
What is the minimum, normal + maximum urine production per day?
Minimum: ~500ml/day
Normal: ~1500ml/day
Maximum: ~20,000ml/day
Diurnal variation
What would happen if someone suddenly ingested 1 L of water?
Big increase in urine volume rapidly to maintain body fluid volume however, amount of solutes excreted remains unchanged so urine osmolarity will decrease, but plasma osmolarity remains constant so cells will not swell
What is the equation for urine osmolarity?
Osmoles excreted/day (Osm) = urine osmolarity (Osm/L) x urine output (L/day)
Explain how urine osmolarity can vary and why it does this.
Urine osmolarity changes according to needs of body to preserve/excrete water. Every day a certain amount of waste solute must be secreted and this can either be done in a small amount of very concentrated urine (>4x [plasma]) or lots of dilute urine (1/6th [plasma])
What is obligatory urine volume? What does it depend on?
Minimum volume of urine that needs to be produced each day to excrete waste solutes
Depends on:
- Max urinary concentrating ability of kidneys (~1200mOsm/L)
- Amount of solutes that need excreting (~600mOsm)
= 600/1200 = 0.5L/day obligatory urine
Why should you not drink salt water on a raft?
If you drink 1L of 1800 mOsm solution: 1800/1200 (max urinary concentrating ability of kidneys) = 1.5 L so you are taking in 1L of water but losing 1.5L -> high levels of solute cause a diuresis even though we are trying to retain water -> more dehydrated
What can cause increased urine volume i.e. polyuria?
Increased water excretion due to excessive water indigestion or inability to concentrate urine (e.g. tubular damage, DI)
Increased solute excretion due to diuretics (or failure to reabsorb Na+) or glycosuria (DM)
What can cause reduced urine volume i.e. oliguria?
Decreased water/solute excretion due to dehydration/low EC volume or poor renal perfusion
Where does reabsorption of water and fine tuning + hormonal regulationoccur in the nephron and what does it require?
Water reabsorption: PT + LOH
Fine tuning + hormonal regulation: medullary collecting ducts
Reabsorption from collecting ducts is passive + requires:
- Insertion of aquaporins (regulated by ADH)
- Osmotic gradient (via countercurrent system in LOH)
For what to be absorbed, filtrate has to be ____ relative to interstitium.
Hypo-osmotic
Where is ADH/vasopressin/AVP produced + transported? What are 2 its functions?
Produced in supraoptic + paraventricular nuclei of hypothalamus -> posterior pituitary -> packaged into storage granules + released by exocytosis (short plasma T1/2)
Functions:
1. Reduce water excretion
2. Vasoconstriction
What 4 factors stimulate ADH release?
- Raised plasma osmolarity (main one)
- Hypovolaemia/low BP/angiotensin II release
- Nausea (‘precaution’ for vomiting + fluid loss)
- Drugs e.g. morphine, nicotine
How will cells in hypothalamus trigger ADH release?
Osmoreceptors will detect increased plasma osmolarity
Peripheral volume receptors will detect hypovolaemia
= ADH release
What is thirst? How does it occur?
Thirst = conscious desire for water
Thirst centres in hypothalamus respond to change in plasma osmolarity + ECV to regulate intake (similar stimuli to ADH release)
What 3 factors inhibit ADH release?
- Reduced plasma osmolarity
- Hypervolaemia/high BP
- Drugs e.g. alcohol
What is the mechanism of action of ADH?
- ADH from blood binds to V2 receptor on collecting duct cell
- IC signalling cascade: ATP -> cAMP -> activates PKA -> protein phosphorylation
- Vesicles with inactive AQP2 channels (synthesized in nucleus) fuse with apical cell membrane
- AQP2 start to reabsorb water from tubular lumen
How does water permeability vary across the nephron?
PT + thin descending LOH: naturally very permeable
CCT/MCT: variable permeability based on ADH presence
Ascending LOH: relatively impermeable in absence of ADH
Where + how is dilute urine formed?
Ascending LOH relatively impermeable to water in absence of ADH so pump moves solutes out of tubule lumen + water cannot follow leaving behind a dilute tubular fluid/hypoosmotic when compared to plasma = dilute urine excreted
Where + how is concentrated urine formed?
DT + CT permeable to water in presence of ADH so water will move so that there is osmotic equilibrium with surrounding interstitium (medullary interstitium is high at ~ 1200mOsm/L/H2O) = concentrated urine excreted
