Control Of Body Fluid Volume + Osmolality Flashcards
Action of angiotensin II
- vasoconstriction of EA
- releases ADH
- stimulates thirst
- causes aldosterone to be released from adrenal cortex > increases Na+ reabsorption from DCT (ENaC)
How do prostaglandins affect Na+ reabsorption?
Decrease in circulating volume stimulates PG synthesis which results in:
- vasodilators > preventing excessive vasoconstriction
- renin release > Na+ reabsorption due to increased aldosterone
How does atrial natriuretic peptide affect Na+ reabsorption
Produced by cardiac atrial cells in response to increased circulating volume > results in:
- inhibit NaK ATPase + closes ENaC channels > reduced Na+ reabsorption
- vasodilation of AE > increases GFR
- inhibit aldosterone secretion
- inhibit ADH release
- decrease renin release
Renal responses to a increase in BP
- Release of ANP: inhibit NaK ATPase + reduced ENaC expression > decreases Na+ reabsorption > increased Na+ + H2O excretion
- increase in hydrostatic pressure of peritubular capillaries: pressure natriuresis + diuresis
Renal responses to decrease in BP
- prostaglandin release
- RAAS activated: AngII > constriction of EA + release of aldosterone > stimulates ADH + thirst | increased expression of ENaC
Renal response in congestive cardiac failure -
- cardiac output falls
- hypotension > Na+ and H2O retention > oedema
- renal hypotension after a fall in CO is sensed by kidneys as hypovolaemia > compensation by retaining NaCl + H2O to increase fluid volume
- increased pulmonary venous pressure > pulmonary oedema
Management of pulmonary oedema due to congestive cardiac failure
Loop diuretics
ACE inhibitors
Vasodilators
Nitrates
Presentation of hypervolemia
- ascites > swelling in abdomen
- pleural effusion
- pulmonary oedema
- peripheral oedema in legs
- coughing
- shortness of breath
- pumping action of heart grows weaker
Causes of hypervolemia
- kidney rotation of sodium + water
- reduced effective arterial volume e.g. congestive cardiac failure
- excessive sodium or fluid intake
- cirrhosis
- hyperaldosteronism
Treatment of hypovolemic shock
Isotonic fluid replacement - saline solution
What is hypertensive renal disease?
High BP caused by narrowing of arteries to kidney
What are hypertensive changes in the kidney
- arteriosclerosis of major renal arteries
- hyalinisation of small vessels with intimal thickening
. - causes chronic ENaC damage + reduced kidney size
Outline the regulation of osmolality
- changes in plasma osmolarity sensed by hypothalamic osmoreceptors
Two pathways initiated:
-ADH in kidneys > affects renal water excretion
-thirst > affects water intake
Where are osmoreceptors located?
Hypothalamus
Actions of ADH when plasma osmolality increases
- blood vessel vasoconstriction: V1 receptor mediated response
- increased water reabsorption: V2 receptor mediated response
What stimulates the thirst response?
Increase in plasma osmolarity
If plasma osmolality decreases, what type of urine is made?
How is this done?
hypoosmotic urine
- decrease ADH conc > decreased aquaporins > decreases H2O reabsorption
- loss of large amounts of dilute urine
If plasma osmolality increases, what type of urine is made?
How is this done?
Hyperosmotic urine
- increase in ADH > increased aquaporins > increased H2O reabsorption in collecting duct
- concentrated urine
What causes a release of renin?
- increased sympathetic innervation
- decrease in BP
- decreased Na+ to macula densa cells
How does a decrease in Na+ activate renin release?
- less Na+ to macula dense
- MD stimulated > secrete prostaglandins
- prostaglandins act on granular cells
- renin released
How do prostaglandins affect Na+ reabsorption?
- vasodilator effect (prevents excessive Vasoconsition)
- act on granular cells to release renin > activates RAAS > increases Na+ reabsorption from DCT
Where does prostaglandin synthesis occur in the kidney?
Cortex
Medullary interstitial cells
Collecting duct epithelial cells
Where are atrial natriuretic peptides produced by?
In response to what?
Caridac atrial cells
In response to increase in ECF volume
How does angiotensin II maintain GFR?
Constricts efferent article > increases pressure in glomerulus
What is SIADH?
Syndrome of inappropriate ADH secretion
Presentation of SIADH
- fluid overload
- weight gain
- low urinary output
- conc. urine
- hyponatremia
What is antidiuresis?
Reduction in renal water excretion
