Chapter 20 powerpoint file

POWERPOINT® LECTURE SLIDE PRESENTATIONby LYNN CIALDELLA, MA, MBA, The University of Texas at AustinAdditional Text by J Padilla exclusively for physiology at ECC

Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings

HUMAN PHYSIOLOGYAN INTEGRATED APPROACH FOURTH EDITION

DEE UNGLAUB SILVERTHORN

UNIT 3

20 Integrative Physiology II: Fluid and Electrolyte Balance


Mass Balance in the Body Homeostasis requires that amounts

gained must be equal to that lost. Ion concentration- need proper

amounts of Na+, Cl-, K+, and Ca2+: nervous, cardiac& muscle function-

imbalances cause problems with membranes of cells that are excitable.

Primarily replaced with thirst & appetite and excreted in urine, sweat, & feces

pH balance- cells functions within a pH range that is maintained by H+, CO2, & HCO3–

Fluid- water levels need to be maintained, ingestion and urine formation have largest impact.


Key factors for Homeostasis

Na+ & H2O= affect ECF Osmolarity: amounts of solutes dissolved in solution, concentration and permeability influence direction of osmosis which changes the size of cells

Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings Figure 5-29

Osmosis and Osmotic PressureOsmolarity describes

the number of particles of solution in a quantity of osmoles OsM per liter

Osmolarity is influence by fluid, ion, & protein levels. Compensation occurs via renal, behavioral, repiratory, and CV responses


Water Balance in the Body Water makes up 50-60% of total body weight.Main entry way is through food, most lost in urine unless there is excessive sweating or diarrheaHomeostasis maintains water balance unless there is pathology or an abnormal ingestion of water. Men have more water than women


Water Balance

A model of the role of the kidneys in water balance

Kidneys cannot add water, only preserve it or get rid of excess amounts. Renal filtration will stop if there is a major loss causing extremely low blood pressure and blood volume


Fluid and Electrolyte HomeostasisThe body’s

integrated response to changes in blood volume and blood pressure incorporate many systems

Decreased blood volume will result in mechanisms that increase blood pressure and volume, and reduce water loss

Figure 20-1a

Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings Figure 20-1b

Fluid and Electrolyte Homeostasis

Increased blood volume results in the excretion of salt and water which eventually reduces blood pressure and ECF/ICF volumes.


Urine ConcentrationOsmolarity changes as filtrate flows through the nephron. Reabsorption is controlled by kidney tissue concentrations as water permeability and diffusion of solutes changes as needed. Water and sodium reabsorption alter urine concentration. Diuresis is the removal of excess water.

Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings Figure 20-5a

Water Reabsorption

Vasopression or antidiuretic hormone causes a graded effect of forming water pores on collecting duct cells. Thus permeability is increased and more water is retained making urine more concentrated.

Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings Figure 20-5b

Water Reabsorption

If vasopressin is absent water will not move out through water pores (aquaporins)and the urine will be dilute.

Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings Figure 20-6, steps 1–2

Water Reabsorption

Collecting duct lumen

Filtrate300 mOsm

Cross-section ofkidney tubule

Collecting duct cell

Secondmessengersignal

cAMP

Medullaryinterstitial

fluid

Vasopressin receptor

Vasarecta

Vasopressin

Vasopressin binds to mem-brane receptor.

Receptor activates cAMP second messenger system.

1 2

1

2

600 mOsM600 mOsM

700 mOsM

The mechanism of vasopressin action on tubular cells of the nephron


Water Reabsorption


Filtrate300 mOsm

Exocytosisof vesicles




cAMP

Storage vesicles

Aquaporin-2water pores


fluid


Vasarecta

Vasopressin



Cell inserts AQP2 water pores into apical membrane.

1 2 3

1

2

3

600 mOsM600 mOsM

700 mOsM

Apical membrane water permeability increases exponentially with water pores are added


Water Reabsorption


Filtrate300 mOsm

H2O

Exocytosisof vesicles




H2O

cAMP

Storage vesicles

Aquaporin-2water pores

600 mOsM

H2O


fluid


600 mOsM

Vasarecta

H2O

700 mOsM

Vasopressin



Cell inserts AQP2 water pores into apical membrane.

Water is absorbed by osmosis into the blood.

1 2 3 4

1

2

3

4

Vassopressin is also called antidiuretic hormone- it causes reabsortion of water (in turn increasing urine concentration and decreasing volume).


Factors Affecting Vasopressin Release

Three stimuli control vasopressin but the most potent is blood osmolarity above 280mOsM. The higher the osmolarity, the more vasopressin released by posterior pituitary. Osmoreceptors also trigger thrist centers in hypothalamus


Water BalanceCountercurrent exchange in the medulla of the kidney. Descending limb is permeable to water while the ascendig limb is permeable to ions. 25% of all Na+ and K+ reabsorption happens in ascending limb; resulting in dilute urine. Water amounts can be changed again at distal tubule and collecting duct.


Fluid and Electrolyte Balance Vasa recta removes water- blood

runs in opposite direction as filtrate, water moves in according to the concentration gradient Close anatomical association of the

loop of Henle and the vasa recta- this allows for water to move out of the tubule and into the blood without dilution the interstitial fluid in the medulla.

Urea increase the osmolarity of the medullary interstitium- transporter proteins move urea into the medulla to increase osmolarity of the interstitial fluid creating a gradient to move water out without affecting the movement of other ions (Na+ & K+)


Sodium BalanceHomeostatic responses to salt ingestion show the integrated effects on sodium, water, and blood pressure. Without salt appetite [salt] would increase and tissue cells would shrink. Thus vasopressin and thirst is activated.

.


Sodium Balance

Interstitialfluid

Blood

Aldosterone

Aldosteronereceptor

P cell of distal nephron

Lumen of distal

tubule

Aldosterone combines with a cytoplasmic receptor.

Hormone-receptor complex initiates transcription in the nucleus.

1

2

12Transcription

mRNA

Aldosterone action in principle cells- targets cells of the distal convoluted tubule and collecting duct.


Sodium Balance

Interstitialfluid

Blood

Aldosterone

ATP

Aldosteronereceptor


Translation andprotein synthesis

ATP

Lumen of distal

tubule



New protein channelsand pumps are made.

Aldosterone-induced proteins modify existing proteins.

1

2

3

4

12

3

4

Transcription

mRNA

Newchannels

Proteins modulateexisting channels and pumps.

New pumps

Existing channels are called the leak proteins that allow for a rapid movement of ions


Sodium Balance

Interstitialfluid

Blood

Aldosterone

ATP

Aldosteronereceptor


Translation andprotein synthesis

K+

Na+

K+ K+

Na+

Na+

ATP

K+

secreted

Na+

reabsorbed

Lumen of distal

tubule



New protein channelsand pumps are made.

Aldosterone-induced proteins modify existing proteins.

Result is increased Na+ reabsorptionand K+ secretion.

1

2

3

4

5

12

3

4

5

Transcription

mRNA

Newchannels

Proteins modulateexisting channels and pumps.

New pumps

Aldosterone causes K+ secretion and sodium reabsorption. A secondary effect is that water follows sodium.


Sodium Balance

Decreased blood pressure stimulates renin secretion. Granular cells can be activated to release renin by three factors: drop in blood pressure, a signal from the kidneys, or increased sympathetic activity.


Sodium Balance

The renin-angiotensin-aldosterone pathway- (RAAS). Renin is an enzyme that assist in ANG II formation. ANGII activates several mechanisms that ultimately increase blood pressure and volume


Sodium Balance

Action of natriuretic peptides- cause sodium loss through urine (natriuresis) and act as RAAS antagonist. They are released when myocardial cells stretch too much or during heart failure


Potassium Balance Regulatory mechanisms keep plasma potassium in narrow range

(3.5-5meq/L) Aldosterone is released in response to excess levels, it increases

permeability at distal nephron so K is moved into the urine while sodium is reabsorbed

Hypokalemia (K+ levels below 3) In ECF levels are low, K+ leaves the cell, and resting membrane

potential is more negative (hyperpolaized)= stronger stimulus Muscle weakness and failure of respiratory muscles and the heart due

to hyperpolarized neurons. Hyperkalemia (K+ levels above 6)

In ECF levels are high, more K+ enters the cell, thus depolarizing it but then less able to repolarize thus LESS excitable

Can lead to cardiac arrhythmias K+ irregularities include kidney disease, diarrhea, and diuretics


Behavioral MechanismsDrinking water and eating salt is the only

way the body obtains these substances, therefore individuals who cannot do this must be assisted.

Drinking replaces fluid loss – when body osmolarity raises above 280mOsM hypothalmic osomreceptors trigger thrist. Oropharynx receptors are stimulated by cold drink and signal thirst quench

Low sodium stimulates salt appetite – the hypothalamus also has centers for salt appetite which trigger a response when osmolarity is low.

Avoidance behaviors help prevent dehydration Desert animals avoid the heat


Disturbances in Volume and Osmolarity

Figure 20-17

In each situation compensantion mechanism aim to bring conditions to normal, in some cases there is incomplete compenstation. Notice how most imbalances are due to what is ingested or loss in excess amounts


Severe Dehydration Compensation Condition: low ECF volume, low blood pressure, high

osmolarity Compensation Mechanisms

Cardiovascular Responses- increase cardiac output & vasoconstriction to increase blood pressure. Vasoconstriction reduces GFR activating granular cells to release renin

Angiotensin II- produce after renin release that activates RAAS pathway to trigger thirst, vasopressin release, and vasoconstrion. (aldosterone is not release as it would increase osmolarity)

Vassopressin- increase water reabsorption to reduce loss in urine

Thrist/ IV-replacement of loss fluids and lowering of osmolarity


Acid-Base Balance Normal plasma pH is 7.38–7.42- also resembles the pH inside

cells, its optimum for proper protein & enzyme function H+ concentration is closely regulated- slight pH changes indicate

a 10-fold increase/decrease in [H+] which can have damaging effects on protein structure & function.

Abnormal pH affects the nervous system- H+ imbalances cause K+ imbalances because transporter protein in kidneys moves H+ and K+ in antiport fashion Acidosis: neurons become less excitable and CNS depression

patients can fall into a coma or have respiratory failure Alkalosis: hyperexcitable- numbness, tingling, muscle twitches,

severe cases lead to paralysis of respiratory muscles pH disturbances- induced by an imbalance of H+ input/output

Compensation by buffers, ventilation, or renal regulation Greatest source is CO2 level changes induced by metabolic or

respiratory factors


Acid-Base BalanceHydrogen balance in the body is quickly compensated by

ventilation and slowly compensated by renal regulation.


Acid and Base InputAcid Organic acids – acids produced by the body during metabolism or

ingested molecules that realease H+ (acidic fruits, amino acids, fatty acids)

Under extraordinary conditions – produce more H+ than the body can normally get rid off and cause pathological effects Metabolic organic acid production can increase Ketoacids –

strong acids produced when fats & proteins are metabolized Diabetes – metabolism disorder causes ketoacid formation

Accumulation of CO2 - can occur as a result of anaerobic respiration, increased metabolism, or decreased ventilation Acid production - CO2 combines with water rapidly to make an

acid and drop pH. Respiratory system gets rid of 75% of aBase Few dietary sources of bases- conditions of alkalosis rarely

encountered


pH DisturbancesThe reflex pathway for respiratory compensation of metabolic acidosis responds to shifts in H+ & CO2 based on the law of mass action. CO2 + H2O == H2CO3 == H+ HCO3 .


pH Homeostasis Buffers moderate changes in pH- cannot prevent changes,

they absorb/release H+ Cellular proteins, phosphate ions, and hemoglobin- serve

as intracellular buffers Ventilation

Rapid- quickly gets rid of CO2 by increasing breathing rate 75% of disturbances- are cleared by ventilation thanks to

the central and peripheral chemoreceptors that sense changes in [H+]

Renal regulation- uses ammonia and phosphate buffers in addition to Directly excreting or reabsorbing H+

Indirectly by change in the rate at which HCO3– buffer is

reabsorbed or excreted


pH Disturbances

Overview of renal compensation for acidosis. The nephron takes care of the 25% of compensation the lungs can’t handle. They excrete H+ by trapping it in ammonia and phosphate ions. They also make HCO3


Intercalated CellsRole of intercalated cells in acidosis and alkalosis – these are located in

between principal cells of the distal tubule and have high amounts of carbonic anhydrase. Movement occurs via H+-ATPase and H+-K+-ATPase


Acid-Base BalanceRespiratory system increases CO2 during hypoventilation and decreases it during hyperventilation. When metabolism causes a disturbance respiratory keeps CO2 levels normal but pH changes because buffer levels drop.

Mass balance shifts equation to left or right

CO2 + H2O == H2CO3 == H+ HCO3 .

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Chapter 20 powerpoint file