Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
12 Cards in this Set
- Front
- Back
|
Learning objectives
|
List the major physiological factors that regulate renal free water excretion
Describe integrated control of free water and sodium excretion that maintains constant composition and volume of plasma and extracellular fluid Describe mechanisms of sodium and water retention in pathophysiological states such as congestive heart failure Describe causes and clinical effects of hyponatremia and the general principles of the treatment |
|
|
Antidiuretic hormone (ADH or vasopressin) and excretion of free water by kidney
|
Acts on principal cells of kidney in collecting duct
On basolateral cells, there are V2 ADH receptors. When stimulated, AQP2 (aquaporin) water channels in vesicles move to apical membrane. AQP3/AQP4 expressed on basolateral side (not regulated, always water permeable) |
|
|
Importance of inner medullary gradient in urinary concentration
|
300 mOsm/kg in cortex to 1200 mOsm/kg in inner medulla
-High osmolarity of medulla is driving force for reabsorption |
|
|
Free water reabsorption depends on two elements
|
1. Pathway with ADH/AQP2
2. Driving force with hyperosmolar medulla |
|
|
Regulation of ADH secretion
|
Plasma osmolarity
-If it increases, osmoreceptors in hypothalamus (PVN, SON) send a message to posterior pituitary which releases ADH (more water is reabsorbed) -If it decreases, osmoreceptors in hypothalamus (PVN, SON) send a message to posterior pituitary which decrease ADH secretion (more water is excreted) Arterial volume -Stretch receptors are located in aortic arch, carotid arteries, and left atrium -A decrease in arterial volume, decreases arterial stretch, and increases ADH secretion (more water is reabsorbed) |
|
|
Changes in volume alter the effect of osmolality on ADH release
|
Plasma osmolality on x-axis
Plasma ADH on y-axis Decrease in volume/pressure shifts curve to left and increases slope -Small changes in osmolality have large effect on ADH Increase in volume/pressure shift curve to right and decrease slope -Small changes in osmolality have a smaller effect on ADH |
|
|
Integrated control of renal sodium and water excretion
|
Integrated response to decreased sodium and water intake
-Decreased arterial filling which decreases vascular strech and cardiac output --Stimulates the sympathetic nervous system which increases sodium retention (increases sodium resorption, renin release), sodium retaining --Stimulates RAAS which decreases sodium excretion through AngII, sodium retaining --Decreases release of ANP along with intrarenal DA and NO, sodium retaining --Increases release of ADH which decreases water excretion -Decreased excretion feeds back by increasing arterial filling Integrated response to increased sodium and water intake -Opposite effect -Increased arterial filling leads to increased vascular stretch and cardiac output -Decreased sympathetic nervous system, RAAS, ADH -Increased ANP and intrarenal DA and NO |
|
|
Underfilling theory of CHF
|
Decreased arterial filling and greatly decreased cardiac output (even with no change in H20 and Na intake)
Essentially sends same message to kidney as if there is low Na and H20 Turns on ADH, SNS, RAAS and turns down ANF, DA, NO Causes them to retain water and Na because low cardiac output sends wrong signal. |
|
|
Causes of arterial underfilling in hepatic cirrhosis
|
Fluid extravasation from liver surface due to increased portal pressure
Arterial vasodilatation Essentially sends same message to kidney as if there is low Na and H20 Turns on ADH, SNS, RAAS and turns down ANF, DA, NO Causes them to retain water and Na because underfilling output sends wrong signal. |
|
|
High ADH due to decreased arterial volume
|
Decreased extracellular fluid volume (hypovolemic hyponatremia)
-Total volume depletion -Appropriate physiologic response --Low arterial stretch increases ADH which decreases free water excretion Increased extracellular fluid volume (hypervolemic hyponatremia) -Patients with generalized edema -CHF, hepatic cirrhosis |
|
|
Syndrome of Inappropriate ADH Secretion (SIADH)
|
SIADH is caused by sustained increase in ADH secretion not due to changes in plasma osmolality (“NONOSMOTIC RELEASE OF ADH”) or arterial volume and with normal endocrine and renal function:
-Carcinomas -Pulmonary disorders -CNS disorders -Infectious diseases (HIV) -Drugs ADH secreted not in response to a stimulus -Increases water reabsorption, decreasing free water excretion --Plasma volume increases which tends to increase sodium excretion (UV) (salt wasting) |
|
|
Clinical consequences and treatment of hyponatremia
|
Altered mental status
-Confusion -Coma -Seizures -Increase risk of falls in elderly Poor prognostic indicator Should not be corrected rapidly otherwise it can cause osmotic demyelination ADH receptor antagonists |
