Kidney Function III, Production of dilute urine Flashcards
Definition of oligouria
Urine output below obligatory water loss of 0.428l/day
Definition of polyuria
Excessive output of urine over 1-2l/day
Definition of polydipsia
Excessive thirst
Definition of nocturia
Having to pass urine at night
What are the 2 ways of maintaining a constant plasma osmolarity
Urine formation
Thirst
What is the equation for osmolar clearance
What is osmolar clearance
What is the fasting osmolar clearance
Cosm = Uosm x urine flow rate / Post
Volume of plasma cleared of osmotically active molecules
2-3ml/min
What is the obligatory osmolar clearance
What is the range of urine osmolarity
600mosmol/l
0.428l/day
50-1400mosmol/l
What is the equation for free water clearance
What is free water clearance
How would you interpret the free water clearance
0<
0=
0>
CH2O = V - (Uosm x V/Posm)
Kidney’s ability to excrete dilute/conc urine
0< dilute
0= isotonic
0> conc
Describe the pathway of action of ADH when dehydrated
Dehydration => increased Posm
Increased signalling from osmoreeptors in OVLT, MPN, SO => paraventricular, supraoptic
Neurohypophysis releases more ADH
Increased water absorption
Describe the pathway of action of ADH when overhydrated
Overhydration => decreased Posm
Decreased signalling from osmoreceptors in OVLT, MPN, SO => paraventricular, supraoptic
Neurohypophysis releases less ADH
Decreased water absorption
What promotes ADH release
Increased Posm
Ang2/decreased BV, BP
Nicotine, nausea, stress, pain
What inhibits ADH release
ANP
Alcohol
What is osmotic diuresis
Small molecules can’t be reabsorbed => increased osmolarity and water retention
Results in polyuria, polydipsia
What is diabetes insidious
What are the 2 types
What are the 2 main symptoms
Neurogenic (no ADH released)
Nephrogenic (faulty V2 rec/AQP2)
Excess thirst
Polyuria
Polydipsia
Nocturia
Describe the importance of potassium How is it reabsorbed/secreted in the -PT -Thick asc LOH -Intercalated cells -Principle cells
Dictates cell resting membrane potential
PT
- Passive reabsorption/FD
- Some secretion via FD, driven by NaKATPase
Thick asc LOH
- NaKCl triporter/passive => cell, driven by NaKATPase
- KCl exchange/FD => medulla
Intercalated cells
-HK exchange => FD => medulla
Principle cells
-ROMK, BK, KCl secretion due to NaKATPase
What are the 4 ways of regulating K secretion in principle cells
Increased Na reabsorption
Aldosterone
-acts on NaKATPase, ENac
Tubular flow rate
-increased flow => more secretion, less reabsorption
pH
- acidosis inhibits (KH intercalated cell activity inhibited)
- alkalosis enhances (NaH stimulated => NaK activated)
What is hypokalaemia
What are the 3 causes
Plasma K < [3.5]
Increased external losses
- increased tubular flow rate
- hyperaldosteronism
Redistribution into cells
- metabolic alkalosis (NaH => NaK)
- excess insulin
Inadequate intake in diet
What are the symptoms of hypokalaemia
Increased K in cell => hyperpolarisation
Larger stimulus needed to reach AP
Longer repolarisation
Affects muscle function
What are the 4 methods of treating hypokalaemia
KCl admin
Consume K rich food
K sparing diuretics (Diuretics inhibit NaK)
Alkalosis correction
What is hyperkalaemia
What are the 2 main causes
plasma K > 5.5
Decreased external losses
- renal failure
- hypoaldosteronism
Redistribution into cells
- metabolic acidosis/lack of insulin/ketoacidosis (NaH inhibited, NaK inhibited)
- Tissue death, released K
What are the symptoms of hyperkalaemia
Why is hyperkalaemia more dangerous than hypokalaemia
Low cell K => depolarisation
Weaker stimuli needed to reach AP
Affect cardiac function => arrhythmias
How would you treat hyperkalaemia
ADRESS THE HEART FIRST
Short term
-Ca admin => keep heart beating
Medium term
-Insulin and glucose admin => K moves into cells
Long term
-K secretion via diuretic
