U1 NUR112 - Fluid & Electrolytes Body Fluid Regulations

Thirst

*Primary regulator of water intake *Plays an important part role in maintaining fluid balance and preventing dehydration

Renin-Angiotensin-Aldosterone System (part 4) RAAS

Angiotensin II stimulates adrenal cortex to release. aldosterone. Aldosterone promotes sodium and water. retention in the distal nephron. of the kidney, restoring blood volume.

Renin-Angiontensin-Aldosterone System (part 3) RAAS

Angiotensin. I travels through bloodstream to lungs where it is converted to angiotensin II by angiotensin-converting. enzyme (ACE). Angiotensin II is a potent vasoconstrictor; it raises the blood pressure. It also stimulates the thirst mechanism to promote fluid intake and acts directly o the kidneys, causing them to retain sodium and water.

Renin-Angiotensin-Aldosterone System (part 2) RAAS

Decreased blood volume and renal perfusion set off chain of reactions leading to release of aldosterone from the adrenal cortex. Increased levels of aldosterone regulate serum K+ and Na+, blood pressure, and water balance through effects on the kidney tubules

Recognize populations at risk across the lifespan for dysfunctions with Fluid & Electrolytes

Elderly: thirst mechanism declines with age Patients with altered mental status/LOC/intubated or artificially fed

Renin

Enzyme that. ism produced by the kidney that converts angiotensinogen (a plasma protein) in the circulating blood into angiotensin I.

Glomeruli

Filter about 170L of plasma every day About 99% of glomerular filtrate is reabsorbed, and only about 1500mL of urine is produced over a 24hr period.

Renin-Angiotensin-Aldosterone System (part 1) RAAS

Helps to maintain intravascular fluid balance and blood pressure. A decrease in blood flow or blood pressure to the kidneys stimulates specialized receptors in the juxtaglomerular cells of the nephrons to produce renin, an enzyme that converts angiotensinogen (a plasma protein) in the circulating blood into angiotensin I.

Atrial Natriuretic Peptide (ANP) (part 1)

Hormone released by atrial muscle cells in response to distention from fluid overload. Affects several body systems including cardiovascular, renal, neural, GI, endocrine systems Primarily opposes the RAAS by inhibiting renin secretion and blocking the secretion and sodium-retaining effects of aldosterone. As a result, ANP promotes sodium wasting and increased urine output.

Atrial Natriuretic Peptide (ANP) (part 2)

Hormone that opposes Renin-Angiotensin-Aldosterone System Stops renin secretion and blocks the secretion and sodium retaining affects of aldosterone Promote sodium waste and increase urine output

Aldosterone (part 2)

Increased levels of aldosterone regulate K+, Na+, blood pressure and water balance through effects on the kidney tubules

Thirst Center

Located in the hypothalamus and is stimulated when blood volume drops because of water losses or when serum osmolality increases. Highly effective in regulating ECF Na+ levels. Increased Na+ in ECF increases serum osmolality, stimulating the thirst center. Fluid intake in turn reduces the sodium concentration of ECF and lowers serum osmolality. A drop in serum sodium and low serum osmolality inhibit the thirst center.

Angiotensin II

Potent vasoconstrictor activated buy angiotensin I which is activated by renin. Angiotensin II raises blood pressure, stimulates thirst mechanism to promote fluid intake and acts directly on kidneys causing them to retain sodium and water Stimulates adrenal cortex to release aldosterone

Kidneys

Primarily responsible for regulating fluid volume and electrolyte balance as they regulate the volume and osmolality of body fluids by controlling excretion of water and electrolytes. By selectively reabsorbing water and electrolytes, the kidneys maintain the volume and osmolality of body fluids

Liver

Produces angiotensinogen in plasma

Antidiuretic Hormone (ADH, Vasopressin) (part 1)

Released by the posterior pituitary gland Regulates water excretion from kidneys Osmoreceptors in hypothalamus respond to increases in serum osmolality and decrease in blood volume, stimulating ADH production and release. Acts on distal tubules of kidneys, making them more permeable to water and increasing water reabsorption.

Aldosterone (part 1)

Released from the adrenal cortex in the adrenal gland Promotes sodium and water retention in the distal nephron of the kidney, restoring blood volume. Essential for sodium conservation in the kidney, salivary glands, sweat glands and colon

Angiotensin I

Small polypeptide generated in plasma by the action of the enzyme renin on angiotensinogen Inactive precursor of angiotensin II Travels through the bloodstream to the lungs where it is converted to angiotensin II by angiotensin-converting enzyme (ACE).

Thirst Mechanism

Stimulated when blood volume drops because o f water losses or when Na+ serum. osmolality increases. Declines with aging, making older adults more vulnerable to dehydration and. hyperosmolality. Patients with altered level of consciousness or who are unable to respond to thirst, such as patients who are intubated or artificially fed are also at risk.

What are several regulatory mechanisms that homeostasis requires to maintain the balance between fluid intake and excretion?

Thirst, kidneys, renin-angiotensin-aldosterone mechanisms, antidiuretic hormone, atrial natriuretic peptide. These mechanisms affect the volume, distribution and. composition of body fluids.

Antidiuretic Hormone (ADH, Vasopressin) (part 2)

With increased water reabsorption, urine output falls, blood volume is restored and serum osmolality drops as the water dilutes body fluids and increased amounts of ADH are released in response to stress situations such as nausea, pain, surgery and anthesis, narcotics and nicotine. Its release is inhibited by alcohol and medications such as phenytoin, as well as by increased blood volume and decreased serum osmolality.