L16,17 Integration of Salt and Water Balance Flashcards
What is the
Kidney helps with water and salt balance.
What is the bodies response to deficit in water
- Water deficit
- increases ECF osmolality- sensed by osmoreceptors in the brain
- Increased ADH secretion (from precursor protein in hypothalamus then stored in posterior pituitary to be released)
- Increased Plasma ADH increases insertion of aquaporins in the distal tubule and collecting duct, increasing H2O reabsorption
What are the physiological stimulus for ADH release vs non physiological
- Osmoreceptors in the supraoptic and paraventricular nuclei fire more when plasma osmolality increased by 1-2%
- Inputs to hypothalamus from the medullary vasomotor centre increase ADH release in response to decrease circulating volume - ECF decrease 7-10%
Non physiological
- Pain, stress, Drugs eg. narcotics, carbamazepine
- Carcinomas, CNS disorders
What is Central and nephrogenic diabetes insipidus and how are they differentiated.
Both are a lack of ADH so cannot concentrate urine.
Central: brain injury, tumour or infection causes problem with hypothalamus or posterior pituitary so inadequate ADH secretion. Treatable with ADH analogues
Nephrogenic: certain drugs, Li+, congenital defect in V2 receptor or aqua-porin means that collecting tubule is unresponsive to ADH. Untreatable
Differentiated by blood test for ADH, water deprivation test- hours and then give ADH for which central DI will have a response but Nephrogenic will not
What is Syndrome of inappropriate ADH secretion - causes, consequences
Caused by brain injury, tumour, anti cancer drugs, lung cancer. There is higher plasma ADH than normal so patient retains water inappropriately. This makes Posm significantly lower than normal which can be dire if water intake is not controlled. So patients are restricted from drinking water and have osm monitored
What are the 3 factors that promote secretion of renin
- decrease in afferent arteriole pressure
- increase symp activity
- decrease in macula densa NaCl delivery
What does Renin do
- Converts Angiotensinogen into Angiotensin 1
- Angiotensin 1 cleave to Angiotensin 2 by ACE enzyme
- Angiotensin 2 goes to AT1 receptors:
- increase aldosterone production->vasoconstriction- constriction efferent arteriole,
increase proximal Na+ reabs-> increase Blood volume
-thirst
increase ADH release
decrease RBF, but maintains GFR
All to increase BP!
b)AT2 receptors: vasodilation
What happens if the right renal artery becomes abnormally constricted what will happen to renin secretion by this kidney and the left one
- Decreased right renal perfusion= decreased afferent arteriole pressure sensed by intrarenal baroreceptor, decreased macula densa flow
- increased renin–> leads to
- elevated systemic angiotensin 2 and increase BP which will both inhibit secretion of renin from the left kidney
What is the steps of action of aldosterone from triggers to release
- Angiotensin 2 and High potassium trigger adrenal glands to make aldosterone.
- Aldosterone binds to mineralocorticoid receptor,
- leads to increased ENAC channels to reabsorb sodium (+ water) from the tubular lumen, as well as increased mitochondrial enzymes and NAKATPases on interstitial side.
What drug treats hyperaldosteronism and will a person become sodium deficient if all adrenal function is lost?
Spironolactone- drug.
No, despite lost of aldosterone, they can lower GFR, alter other factors that influence tubular sodium reabsorption to compensate partially for decreased aldosterone dependent sodium reabsorption
Which one is more important regulation of osmolality or regulation of ECF volume? How are they regulated and what is the range
Osmolality- regulated by renal water handling - 1-2%. Mediated by ADH. Because drawing water from ICF volume in brain cells causes cell shrinkage/expansion.
ECF volume is regulated by Na+ handling and varies throughout the day. Mediated by renin-angiotensin and symp NS to help reabsorb Na+ when ECF volume is low.
What mechanisms are activated when ECF volume is already high
Decreased Na+ reabsorption by:
- ANP released from the atria in response to increased filling pressure and increased atrial stretch (venous return).
- It decreases Na+ reabsorption in the DT and outer medullary CT by blocking ENac and inhibition NaKATPase.
- It inhibits the release of aldosterone, renin
- Vasodilates afferent arteriole to increase GFR
+ decreased Symp ns, dopamine and prostaglandins
What are the effects of surgical removal of a kidney that has a blocked renal artery
There is reduced drive for Angiotensin 2 to increase Bp so Bp decreases and serum creatinine goes down
