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BCC A&P 2: Chpt. 27 - Fluid, Electrolyte, and Acid-Base HomeostasisDr. Jeffrey Weisburg PPT Presentation

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Urinary System: Fluid and Electrolyte Balance

• Cover Slide – Cartoon image and caption have been removed (intellectual property and/or syndicated material).

Concept of Balance

• For homeostasis to be maintained, what enters the body and what is produced in the body must equal the sum of what is used by the body and what is eliminated

• Kidneys concern themselves with regulating fluid and electrolyte balance, as well as acid-base balance

Material exchanges affecting plasma content

Solute and water balance• Remember, kidney filter 180L of plasma a day• About 70% of this filtered material is reabsorbed in the

proximal tubule without any regulation• Body can regulate the remaining filtered water and sodium to

vary the amount excreted or retained based on the body’s needs

• Kidney also regulates K+ and calcium as well as acid-base balance

• Regulation of renal excretion mostly take place in the late distal tubules and the collecting ducts

• Two types of epithelial cells line these tubules– Principal cells: involved in water and electrolyte balance under

hormonal control.– Intercalated Cells: involved in acid-base balance

Water Balance

Water Balance

• Control of urinary water excretion is important in regulating plasma volume and osmolarity

• Plasma volume is directly related to blood pressure (high volume equals high pressure and vice versa)

• For osmolarity: an increase in plasma water with no increase in solutes will decrease osmolarity

• Changes in plasma osmolarity affect the movement of water between intracellular fluid and extracellular fluid

Link between blood volume and blood pressure

Osmolarity and the Movement of Water

• If a person drink a significant quantity of pure water, plasma volume will increase and the concentration of solutes in the plasma will decrease.

• Unless the osmolarity is corrected, cells will begin to swell.• If the cells swell to much, will affect the brain causing

alteration in neurological sensitivity– Headaches– Nausea– Confusion– Seizures– Coma– death

Water Intoxication

Electrolyte and protein anion concentration in plasma, interstitial fluid,

and intracellular fluid

Homeostatic response to eating salt

Water Reabsorption in the Proximal Tubule

• As sodium is the main solute in the extracellular fluid and most of the filtered sodium is reabsorbed in the proximal tubule, sodium is the solute that is primarily responsible for producing the osmotic gradient that drives water reabsorption

Mechanism of water reabsorption

The Medullary Osmotic Gradient

Countercurrent Multiplier

• The properties of different portions of the loops of Henle of juxtamedullary nephrons are imperative to the countercurrent multiplier and establishment of the osmotic gradient in the renal medulla

• The term countercurrent refers to the fact that fluid flowing through the descending and ascending limbs, which parallel one another, run in opposite directions

How the countercurrent multiplier created the medullary osmotic gradient

How the countercurrent multiplier created the medullary osmotic gradient

How the countercurrent multiplier created the medullary osmotic gradient

How the countercurrent multiplier created the medullary osmotic gradient

Role of Urea in the Medullary Osmotic Gradient

• The countercurrent multiplier establishes the osmotic gradient by additional solutes are needed to maintain the gradient

• One such solute is urea, a waste product produced during the catabolism of proteins

• Urea can easily move through the membrane so distributes itself equally across them

• In the collecting ducts, it is actively transported out of the tubules and comprises about 40% of the osmolarity of the medullary osmotic gradient

Mechanism of urine concentration in the long-loop juxtamedullary nephrons

Role of the vasa recta in preventing dissipation of gradient

Water reabsorption in the distal tubule and collecting duct

• 70% of water filtered is reabsorbed in the proximal tubules• 20% is reabsorbed in the distal tubules• Remaining 10% is reabsorbed in the collecting tubules• Inside distal tubule, the fluid is hypo-osmotic to the

peritubular fluid• As fluid moves down the collecting duct, osmolarity of the

lumenal fluid is always less than the increasing osmolarity of the medullary interstitial fluid, thus increasing the osmotic force for water to move the renal tubules into the interstitial fluid

• When water is able to go through the walls of the collecting duct, then water is reabsorbed.

Water reabsorption across late distal tubule and collecting duct

Formation of Dilute Urine

Water reabsorption across late distal tubule and collecting duct

Effects of ADH on water reabsorption

• Whether the late distal tubules and collecting ducts are permeable to water will determine if the urine will be dilute (100mOsm) or concentrated (1400 mOsm)

• ADH regulates the permeability of the late distal tubules and collecting ducts to water

Water reabsorption in the absence of ADH

Water absorption in the presence of ADH

Water absorption in the presence of ADH

Stimulation of ADH release

Sodium Balance

• Sodium need to be regulated because it is– Critical to the function of excitable cells– Used to transport other solutes– Primary solute in extracellular fluids

• High levels of sodium in the blood called hypernatremia

• Low levels of sodium in the blood called hyponatremia.

• Sodium is filtered, undergoes tubular reabsorption, but it is not secreted

Mechanism of sodium reabsorption in the proximal tubules

Mechanism of sodium reabsorption in the distal tubules

Aldosterone controls sodium balance

• Reabsorption of Na+ in the distal tubules and collecting duct is regulated by aldosterone

• Aldosterone is synthesized in the adrenal cortex• Secreted into the blood and transported via

protein carriers in the blood• The primary site for the action of aldosterone is the

last 1/3 of the distal tubule and cortical collecting duct on the principal cells

Effects of aldosterone on principal cells of the distal tubule and collecting duct

Renin-angiotensin-aldosterone system

Mechanisms by which angiotensin II increase mean arterial pressure

Mechanism by which a decrease in mean arterial pressure stimulates renin release

Atrial Natriuretic Peptide

Dehydration

Severe Dehydration

Acid-Base Balance• Hydrogen ion concentration or pH of arterial blood is

regulated by both the lungs and kidneys• Need to keep pH between 7.38-7.42• Changes in pH as little as a few tenths of a unit can

have a profound effect on the body– Change conformation shape of protein– Effect nervous system

• Acidosis: decreased excitability of neurons, leading to confusion, coma and death

• Alkalosis: increases the excitability of neurons– Acidosis causes arrhythmias and vasdilation of blood

vessles to the skin

Acid-Base Balance• The body copes with changes in pH by– buffers– Ventilation– renal regulation of H+ and HCO3-

• Buffers are a first line of defense and are always present

• Ventilations is the second line of defense and is a very rapid reflex, taking care of ¾ of the pH disturbances

• Kidneys- are a slower response but very effective with dealing with pH problems

Negative feedback of blood pH by the respiratory system

Respiratory Disturbances

• Respiratory acidosis or alkalosis results from an excess or deficit of carbon dioxide in the blood

• Respiratory acidosis results from lung diseases that interfere with the exchange of carbon dioxide between the blood and alveolar air or from hypoventilation

• Respiratory alkalosis results from hyperventilation, which is very fast breathing causing PC02 to decrease

Metabolic Disturbances

• Are disturbances in blood pH caused by something other than abnormal PCO2.

• Can by caused by excess elimination from the body of alkaline substances like bicarbonate, excess production of acid in metabolism or excess of consumption of acids in the diet

Metabolic Disturbances• Factors contributing to metabolic disturbances– High protein diet: lead to metabolic acidosis due to

production of phophoric acid– High fat diet: produces fatty acid when triglycerides are

broken down (acidosis)– Heavy Exercise: production of lactic acid leading to

acidosis– Excessive vomiting: loss of acids leading to alkalosis– Severe diarrhea: loss of bicarbonate leading to acidosis– Alterations in renal functions: can lead to either acidosis or

alkalosis.

Reflex pathway for respiratory compensation of acidosis