Anatomy: Final Material part 1

Collecting Duct Concentrates Urine

CD begins in the cortex where it receives tubular fluid from several nephrons

passes through medulla, it can reabsorb water and concentrate urine up to 4x

several factors enable the collecting duct to produce hypertonic urine

Collecting Duct Concentrates Urine: Factors that enable CD to produce hypertonic urine

countercurrent anatomy

ascending limb reabsorbing NaCl but not permeable to water

trapping urea in medulla

loops of vasa recta

Countercurrent Multiplier

recaptures NaCl and returns it to renal medulla

maintaining an osmolarity or salinity gradient

loop of henle

fluid is flowing opposite directions in two adjacent tubulues in loop

*loop multiplies salinity --> known as multiplier in deeper medulla

Countercurrent Multiplier: Loop of Henle: Length

length is related to environment

*longer loop allows: greater gradient, more concentrated urine

ex: fish & amphibians: short to no loops

mammals: tend ot have moderate length loops

ex: desert mammals: very long loops!

Countercurrent Multiplier: Ascending limb thick segment

reabsorbs Na, K, and Cl out of lumen into tissue fluid

impermeable to water

interstitial fluid surrounding ascending limb of medulla becomes more hypertonic compared to tubular fluid

tubular fluid becomes more dilute

no salt pumps in thin segment

Countercurrent Multiplier: Recycling of Urea: Deep Medulla

some urea in CD leaves lower end of medullary collecting duct by facilitated diffusion into the tissues

movement of the urea back into the deep medulla helps make its tissue more concentrated by adding to the tissue fluid osmolarity

Countercurrent Multiplier: Recycling of Urea: PCT and DCT

Urea contributes to osmolarity gradient, some urea is reabsorbed at PCT and DCT

urea leaves medulla tissue and enters the lower loop

*thick segment is not permeable to salt

Countercurrent Multiplier: Recycling of Urea: Bowman's Capsule

Urea reabsorbed, secreted into tubule and reabsorbed with some always being added to filtrate at Bowman's capsule and some being excreted inurine

Countercurrent Multiplier: Descending limb thin segment: lumen to tissue fluid

passes through environment of increasing osmolarity

reabsorbs water but not salt

water flows by osmosis out of the tubule lumen into surrounding tissue fluid

Countercurrent Multiplier: Descending limb thin segment: deeper into medulla

osmolarity difference at each horizontal level is multiplied as fluid goes deeper into medulla

fluid in tubule and surrounding tissues is very concentrated at bottom of loop

Control of Water loss: Producing Hypotonic urine

water remains in the tubule as move up the ascending limb, fluid becomes more dilute (has osmolarity lower than blood plasma)

Control of Water loss: Producing Hypotonic urine: If water levels in body are excessive...

Water diuresis occurs in which a large volume of hypotonic urine is excreted

cortical portion of CD continues to actively reabsorb NaCl but is normally impermeable to water without ADH

*No ADH>more salt removed from cortical CD, dilate urine

Control of Water loss: Producing Hypertonic Urine: Dehydration

Dehydration>increase ADH>increase aquaporin channels in CD, increase CDs water permeability

Control of Water loss: Producing Hypertonic Urine: Cortical Portion

in the cortical portion of the CD, water reabsorption occurs by diffusion from the hypotonic fluid in the tubule lumen into the surrounding tissue

Control of Water loss: Producing Hypertonic Urine: Isotonic Tubular Fluid

Isotonic Tubular Fluid then enters and flows down through medullary collecting duct

osmolarity of surrounding interstitial fluid is 4x as high in lower medulla as in cortex, more water reabsorbed by osmosis, urine is more concentrated

Control of Water loss: Producing Hypertonic Urine: When water is again available

tubule cells remove aquaporins from the plasma membrane

install aquaporins into luminal side of tubule cells

ADH does not effect water reabsorption in any part of collecting duct

Countercurrent Exchange System

*Kidney receives blood without destroying osmolarity gradient

Formed by vasa recta

descending capillaries

ascending capillaries

Countercurrent Exchange System: Vasa Recta

gives back salt & subtracts from gradient

provides blood supply to medulla

flows in opposite directions in adjacent parallel cap. but parallel to nephron loops and CD

prevents washing away of osmolarity gradient

Countercurrent Exchange System: Descending Capillaries

water diffuses out of blood

NaCl difusses into blood

Countercurrent Exchange System: Ascending Capillaries

water diffuses into blood

NaCl diffuses out of blood

Acid-Base Balance: pH range

Normal pH range of extra cellular fluid and blood is 7.35 to 7.45

Acid-Base Balance: Homeostasis

Important part of homeostasis: cell metabolism depends on enzymes, and enzymes are sensitive to pH

Acid-Base Balance: Challenges

metabolism produces lactic acids, phosphoric acids, fatty acids, ketones and carbonic acids

*pH determined by concentration of H+ > pH = -log [H+]

Acid-Base Balance: Acids

strong acids ionize freely; release H+ and greatly lower pH

weak acids ionize only slightly, hold onto most protons, weak effect on pH

Acid-Base Balance: Bases

strong bases absorb H+ and greatly raise pH

weak bases bind less of the available H+ and has less effect on pH weak bases bind less of the available H+ and has less effect on pH

Buffers

A chemical buffer does not eliminate H+ from the body or add proteins to the body, it temporarily locks them up until acid-balance is restored

Buffers: Resist changes in pH

substance that can reversibly bind protons

resists changes in pH by removing or adding protons to the system

Buffers: Physiological buffer

-system that controls output of acids, bases or CO2

-->urinary system buffers greatest quantity, takes several hours

-->respiratory system buffers within minutes, limited quantity

Buffers: Chemical Buffer Systems

buffer systems consist of a weak acid and weak base

restore normal pH in fractions of a second

3 major chemical buffer systems:

1. bicarbonate

2. phosphate

3. protein

Bicarbonate Buffer System

Solution of carbonic acid and bicarbonate ions

*key single most important buffer in blood

Reversible reaction important in ECF/blood

Bicarbonate Buffer System: HC03-

HCO3- acts as weak base

CO2 + H2O <- H2CO3 <- HCO3 + H+

*raises pH by binding H+ and removing it from solution

CO2 + H2O -> H2CO3 -> HCO3 + H+

*lowers pH by releasing H+ and adding it to solution

-> here carbonic acid acts as weak acid

Bicarbonate Buffer System: Respiratory and Urinary System

raise pH: kidneys excrete H+ and lungs excrete CO2

lower pH: kidneys excrete HCO3-

-shift reaction to left (lose proton)

-shift reaction to right (gain proton)

as every HCO3 produced fro loss of bicarbonate ion, also produces protons

Phosphate Buffer System

As in bicarbonate system, reactions that proceed to the right release H+ and lower pH, and those to the left, bind H+ and raise pH

Phosphate Buffer System: ICF and renal tubules

Important in ICF and renal tubules

where phosphates are more concentrated

less important in blood and tissue fluids

Protein Buffer System

more concentrated than bicarbonate or phosphate systems especially in the ICF

protein buffering accounts for 3/4 of all chemical buffering

proteins mostly function as buffers in ICF not in blood

(buffering is most fluid and proteins are in ICF)

Acid-Base & Potassium Balances: Acidosis: H+ diffuses into cells and K+ diffuses out

H+ buffered by protein in ICF, so net loss of positive; causes membrane hyperpolarization, nerve and muscle cells are hard to stimulate; CNS depression may lead to death

Acid-Base & Potassium Balances: Acidosis: Net loss of cations inside

Net loss of cations inside -> lose K+ and increased polarity across membrane -> RMP -> more negative

-tends to shut down voltage regulated Na+ gates -> Na+ does not diffuse in (hyperpolarizing)

Acid-Base & Potassium Balances: Alkalosis

H+ diffuses out of cells and K+ diffuses in, membranes depolarized, nerves overstimulate muscles causing spasms, tetany, convulsions, respiratory paralysis

-gain is positive inside cell -> shift RMP closer to threshold

Disorders of Acid-Base Balances: Respiratory Acidosis and Alkalosis

Acidosis: rate of alveolar ventilation falls behind CO2 production

Alkalosis: CO2 eliminated faster than it is produced

Disorders of Acid-Base Balances: Metabolic Acidosis

Increased production of organic aids (lactic acid, ketones seen in starvation and diabetes)

loss of base (chronic diarrhea)

Disorders of Acid-Base Balances: Metabolic Alkalosis

-loss of acid (chronic vomiting)

Renal Control of pH

Most powerful buffer system (can neutralize more acid or base than either the respiratory system or chemical buffers) but slow response

Renal Control of pH: Renal tubules add or eliminate

Kidney's renal tubules eliminate from or add H+ back to body by altering bicarbonate concentration

*excretion of HCO3 in urine, increase H+ in plasma, like you added H+

*adding HCO3 plasma lowers H + in plasma, as if you are removing protons

Renal Control of pH: Bicarbonate filtered at renal corpuscle

Bicarbonate is filtered at the renal corpuscle and is reabsorbed at the PCT, ascending nephron loop and cortical CD

-> bicarbonate is also secreted into (less than absorbed) tubular fluid at DCT and cortical CD

Renal Control of pH: excretion of bicarbonate

Excretion of bicarbonate is filtered bicarbonate minus reabsorbed bicarbonate

--> reabsorbing bicarbonate is not a simple pumping process at either the luminal or basolateral side (toward luminal)

Renal Control of pH: excretion of bicarbonate: secreted ions

Secreted hydrogen ions are bumped into lumen from tubule cells in several tubular segments by Na H antiports or H ATPase pumps

Renal Control of pH: Brush Border of PCT

In the PCT, brush border in the lumen has carbonic anhydrase, which helps generate carbon dioxide and water from bicarbonate and protons in the lumen,

Renal Control of pH: Tubule Epithelial Cells

CARBON DIOXIDE, not bicarbonate enters the tubule epithelial cells from the lumen

*Every CO2, absorbed into cell, can generate a HCO3- and H+ in cell

-bicarbonate is than reabsorbed into blood

Renal Control of pH: Bicarbonate Reabsorption in lumen

While bicarbonate is not directly reabsorbed from lumen, the new bicarbonate formed in cell is like reabsorbing bicarbonate

-->bicarbonate diffuse out of the cell into tissue fluid (facilitated diffusion)

Renal Control of pH: Filtered

Bicarbonate ions are normally filtered by the glomerulus, gradually disappear from tubular fluid as bind with protons to form CO2 and water, and reabsorbed into the peritubular capillary blood from tissue fluid

Renal Control of pH: Normal Conditions

Under normal conditions of normal acid-base balance, all bicarbonate ions in the tubular fluid are consumed by neutralizing hydrogen ions secreted into lumen.

Limiting pH: Tubular Secretion of H+

if H+ concentration increases in tubular fluid, lowering pH to 4.5, secretion of H+ stops

more H+ in urine than bicarbonate -> pH 5-6

*phosphate and ammonia buffers prevent pH from falling too low

Limiting pH: Addition buffers in tubular fluid

phosphate system

ammonia

Limiting pH: Addition buffers in tubular fluid: Phosphate System

Na2HPO4 + H+ --> NaH2PO4 + Na

acts as a base and accepts protons, neutralizing

Limiting pH: Addition buffers in tubular fluid: Ammonia

From amino acid catabolism

NH3 + H+ and Cl- --> NH4Cl (ammonium chloride)

Limiting pH: Addition buffers: Functions

Non bicarbonate buffers allow for bicarbonate to be made in tubule epithelial cells and added to plasma with a net gain of bicarbonate to plasma which alkalinizes plasma, gain of bicarbonate added to plasma lowers proton level back to normal

Compensation for pH balances: Pulmonary Ventilation and Kidneys

Changes in pulmonary ventilation correct pH of the body fluids by expelling or retaining CO2

Kidneys compensate for pH imbalance due to respiratory tissue

*Respiratory system and kidney work together to compensate for pH imbalances of metabolism origin

Compensation for pH balances: Respiratory System Effectiveness

Effective in correcting acid imbalances due to abnormal PCO2, less effective if acid is from metabolic source, ex: lactic acid, ketones

Has rapid, strong buffering effect, can keep proton concentration from changing too much (until kidneys can help)

Compensation for pH balances: Respiratory system: Acidosis and Alkalosis

For metabolic acidosis (until kidneys secrete protons in urine) increase H+

For metabolic alkalosis (reflex drops in ventilation rate) increase CO2, H+

Compensation for pH balances: Renal Compensation (slow, powerful compensation)

adjust pH by changing rate of bicarbonate reabsorption and H+ secretion to tubule fluid

Compensation for pH balances: Renal Compensation (slow, powerful compensation) : Acidosis

renal tubules increase rate of H+ secretion and production of non bicarbonate ions

Allows more bicarbonate to be added to plasma-> lowers the plasma hydrogen ion concentration

*more HCO3 in ECF, shift left, pulling out H+, bring H+ down to normal

Compensation for pH balances: Renal Compensation (slow, powerful compensation) : Alkalosis

HCO3 concentration and pH of the urine elevated as HCO3 is excreted because little is reabsorbed

*protons not secreted in ECF>shift right>CO2 + water produce more HCO3 & more protons, with HCO3 in plasma, plasma hydrogen ion conc. rises

Fluid Compartments

Body water is distributed among certain fluid compartments separated by selectively permeable membranes: Intracellular Fluid and Extracellular Fluid

Fluid Compartments: ICF

65%

Fluid Compartments: ECF

25% tissue flood

8% blood plasma, lymph

2% transcellular fluid (cerespinal, synovial, peritoneal, and other fluid kinds in organs and through the body)

Water and Electrolyte Movement

Fluid is continually exchanged between compartments by the way of capillary walls and plasma membranes

Water and Electrolyte Movement: Osmotic Gradients

Because water moves so easily, osmotic gradients between ICF & ECF don't lost for long

*osmosis from one compartment to another > relative conc. of solutes in each compartment

*as osmolarity in tissue rises, water leaves cells & vice versa

Water and Electrolyte Movement: Abundance

Electrolytes are most abundant solute particles particularly sodium in ECF and potassium in ICF

*electrolytes have same relative concentration in the tissue fluid and blood

Water and Electrolyte Movement: Water Balance

Water balance is maintained when total gain = total loss

Water in Movement in Fluid Compartments

Electrolytes play principle role in water distribution and total water content

Water Movement: Water Gain

Preformed water: ingested in food and drink

Metabolic water: by product of aerobic metabolism an dehydration synthesis

Water Movement: Water Loss

Routes of loss: urine, cutaneous transpiration, expired breath, fecal matter, sweat (during evaporative cooling)

*water diffuses out of epidermis: it is not released from evaporating cooling

Loss varies greatly with environment and activity

Regulation of Fluid Intake: Controlled by

Hypothalamic osmoreceptors

ADH

AGII

*produce a conscious sense of thirst

*thirst also inhibits salivation

Regulation of Fluid Intake: Hypothalamic

Hypothalamic osmoreceptors; signal in response to increaseing ECF osmolarity

->signal cerebral cortex: signal thirst

Regulation of Fluid Intake: ADH

produced in response to increased blood osmolarity

Regulation of Fluid Intake: Angiotensin II

produced in response to decreased Blood Pressure

-->also response to decreased blood volume, increase osmolarity

Regulation of Fluid Output: Water Excretion

Regulation of fluid output is accomplished by varying urine volume

Water excretion is the difference between volume of water filtered and volume reabsorbed

Regulation of Fluid Output: Kidney

In kidney, changes in urine volume are usually linked to adjustments in sodium reabsorption

As sodium is reabsorbed or excreted in nephron tubule, water accompanies it

Kidneys cannot replace lost water or electrolytes, but can slow down water loss

Regulation of Fluid Output: ADH

Provides a means of controlling water output independently of sodium

Regulation of Fluid Output: Baroreceptors

When a significant decrease in blood pressure occurs, which causes baroreceptors to send signals to hypothalamus to cause posterior pituitary to release ADH

Regulation of Fluid Output: ECF volume changes

ECF volume changes often associated with loss or gain of Na & H2O in proportional amounts

In contrast, changes in total body H20 with no corresponding change in total body Na are compensated for by altering H2O excretion without Na excretion

Regulation of Fluid Output: Total Volume

Total volume of fluid in body body may change but osmolarity in ECF will not change, END: changes in water alone in contrast to changes in Na, have little effect on ECF-->water unlike Na moves out of ECF and into ICF

Electrolytes: Function

chemically reactive in metabolism

determine cell membrane potentials

affect osmolarity of body fluids

affect body's water content and distribution

Electrolytes: Major Cations and Anions

Cations: Na, K, Ca, H (Na most important)

Anions: Cl, HCO3, PO4

Sodium Functions: Membrane and ECF

Responsible for resting membrane potentials of cells, & its inflow is an essential event in nerve & muscle function

Principle cation of ECF, along with chloride, are about 85-90% of solutes

Sodium Functions: Gradients

Sodium gradients across plasma membrane also provide the potential energy involved in cotransport of glucose, chloride, K, and Ca

*Even though Na enters cell through ion channels

*Na behaves as if it is non-penetrating ion -> cannot pass into cell

Sodium Homeostasis: Excretion and Secretion

Sodium excreted = Sodium filtered - sodium reabsorbed

Sodium is not secreted

*Water follows sodium into the tissue fluid

Sodium Homeostasis: Macula Densa

Decreased sodium concentration in blood leads to decreased sodium concentration in tubular fluid, which macula dense defects

macula densa--> cause JG cells to release renin

Sodium Homeostasis: ADH and aldosterone

Unlike ADH, aldosterone does not change ECF sodium concentration

Angiotensin II also directly increases sodium reabsorption

Sodium Homeostasis: Aldosterone

Aldosterone = key hormone in Na+ regulation, increase Na-K and DCT and cortical CD

Aldosterone -> stimulates Na Reabsorption in large intestine and ducts of sweat glands

Sodium Homeostasis: Renin-Angiotensin-Aldosterone Mechanism

Increased blood volume and increased blood pressure inhibits the renin-angiotensin-aldosterone mechanism

Sodium Homeostasis: ANP

Rise in BV an BP causes ANP release which inhibits aldosterone and renin release

ANP works to inhibit sodium reabsorption in tubular segments

Thus, increase in urine volume, decrease BV, and decrease BP

Potassium - Functions

Most abundant cation of ICF

determines intracellular osmolarity

membrane potentials (with sodium)

->cofactor: key to protein making and other metabolic actvities

Potassium - Homeostasis: Glomerular Filtrate

Almost all K+ in glomerular filtrate is reabsorbed by PCT

DCT and cortical portion of collecting duct secrete K+ in response to blood levels

Increased blood K+ levels directly stimulate adrenal cortex to release aldosterone

Potassium - Homeostasis: Aldosterone

Aldosterone stimulates more renal secretion of K+ via more Na-K+ pumps

K+ excretion is controlled by K+ return rate in DCT

ex: k+ increases, increase K+ secretion in filtrate

k+ decrease, decrease K+ secretion in filtrate

Potassium Imbalances: MOST DANGEROUS IMBALANCES OF ELECTROLYTES: Hyperkalemia (effects depend on rate of imbalance)

sudden increase of K+ outside cells leads to more positive in cells and closer to threshold, makes nerve/muscle/heart muscle cells abnormally excitable

slow onset inhibits repolorazation cause nerve & muscle to become less excitable

Potassium Imbalances: Hypokalemia

causes more K+ to leave cells and ICF, and cells become hyperpolarized

Nerve/muscle/heart cells are less excitible

*during slow onset hyperkalemia, ECF potassium levels increase slowly

Anatomy: Final Material part 1

Health Science 1202 with Ricahrdson at Northeastern University

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