AHP2 Exam Flashcard Set

In an arteriole, what is the hydrostatic pressure at the entrance versus the exit?

At the entrance the HP is 80mmHg and at the exit it is 35mmHg.

What is the hydrostatic pressure at the entrance and exit of a capillary?

At the entrance the HP is 35mmHg and at the exit it is 15mmHg

What is the hydrostatic pressure at the entrance of a venule?

15mmHg

What is the pressure in the ISF surrounding a capillary?

0 mmHg

How does the pressure difference between the inside of the capillary and the outside of the capillary affect the flow of water?

It pushes water out

If water is constantly getting pushed out of the capillary due to the pressure difference between the capillary and the ISF, why do we not swell up?

While water is getting pumped out the concentration of solute (plasma proteins) in the lumen is increasing which cause water to come back in as a result of osmosis. This balances the water efflux.

What is colloid osmotic pressure?

It is osmosis that is occurring due to the increased concentration of plasma proteins in the lumen of the capillary.

What is the value of the colloid osmotic pressure?

25mmHg

If the colloid osmotic pressure is balancing the water efflux, why does the hydrostatic pressure decrease by the time it reaches the venule?

There is always a net loss as a little bit of water is always entering the ISF.

What happens to the excess water that is pushed out of the capillaries?

It gets taken up by the lymph capillaries

How does elephantiasis cause an edema?

A worm lives in the lymph capillaries which prevents the uptake of excess water causing the leg to get bigger.

During reabsorption in the proximal tubule, what are the ways that sodium gets moved out of the lumen?

Sodium Channels (luminal membrane), Na/K ATP pump (basolateral membrane), Na/AA symport carrier (luminal membrane), and Na/Glucose symport carrier (luminal membrane)

What happens to the concentration of glucose and amino acids in the lumen of the proximal tubule during reabsorption?

They get completely removed using the sodium gradient.

Why and how is chlorine moving during reabsorption in the proximal tubule?

Due to the exit of sodium, the lumen becomes more negative which allows chlorine to flow down its electrical gradient across the luminal and basolateral membranes.

Why and how is water moving out of the proximal tubule during reabsorption?

Due to the efflux of solutes, the solute concentration decreased, and the water concentration is increased causing water to go through aquaporins via osmosis through both the luminal and basolateral membrane.

How does the hydrostatic pressure increase in the intercellular fluid (space) and what does it cause?

The influx of water and solutes into this space increases the hydrostatic pressure which pushes fluid containing these solutes into the ISF.

How does the fluid pushed out of the intercellular space in the proximal tubule get moved into the peritubular capillaries?

When the fluid is pushed out of the proximal tubule, it increases the hydrostatic pressure in the ISF which then pushes the fluid into the lumen of the peritubular capillaries.

How and why is potassium pushed out of the lumen of the proximal tubule?

The exit of water increases the concentration of potassium in the lumen which allows it to flow down it’s concentration gradient across the luminal and basolateral membrane.

How and why is H₂PO₄ moved out of the lumen of the proximal tubule?

Due to the water exit, the concentration increases inside the lumen which allows it to flow down it’s concentration gradients through channels in the luminal and basolateral membranes.

How and why is calcium moved out of the lumen of the proximal tubule?

The water exit increases calcium concentration in the lumen allowing calcium to flow down its concentration gradient through calcium channels in the luminal membrane, it is then pushed across the basolateral membrane using the calcium ATPase.

How does K+, H2PO4, and Ca+ get pushed into the peritubular capillaries?

Once they are in the intercellular fluid, the hydrostatic pressure pushes them out of the proximal tubule into the ISF which increases the hydrostatic pressure there, ultimately pushing it to the peritubular capillaries.

What is the main difference between the types of pumps/ modes of transport used during reabsorption in the proximal tubule?

Everything is passive except for the Na/K pump and the Ca pump.

What does it mean to be isoosmotic?

The concentration of water and solute is the same.

In the plasma/blood what is the standard osmolarity?

300mOsm

Why is it still 300mOsm at the end of the proximal tubule if the volume is less?

Because water and solute leaves at the same rate.

What is the osmolarity inside the proximal tubule?

300mOsm

What happens to the osmolarity in the descending part of the loop of Henle?

It increases the further down it goes

What percent of K+, Ca++, and H2PO4 is reabsorbed in the proximal tubule?

90%

If 90% of the water is removed from the proximal tubule, what happens to the concentration of potassium calcium, and H2PO4?

They are increased tenfold.

How does osmolarity effect the color of urine?

The closer it is to 50, the clearer the urine is

Of the collecting duct system, what is located in the cortex and what is located in the medulla?

Cortex: proximal tubule, distal tubule, and the cortical collecting tubule

Medulla: Ascending and Descending loop of Henle and the medullary collecting tubule

How do the peritubular capillaries differ in the cortex and the medulla?

the capillaries have bigger loops in the medulla

What is the osmolarity range in urine?

50mOsm to 1500mOsm

Why is water leaving the lumen of the descending loop of Henle?

Since the osmolarity is greater in the ISF than in the lumen, the water is going down its gradient through aquaporins.

Why can’t sodium move into the ISF from the lumen in the descending loop of Henle?

There are no sodium channels open and there is very little of Na/K pumping

Why is Cl not moving out of the descending loop of Henle?

Since there is no sodium efflux the lumen is not generating a more negative charge, so it doesn’t need to move

What is happening to the osmolarity in and out of the descending loop of Henle?

In the ISF, the osmolarity is increasing all the way to 1500, inside it is also increasing to 1500 but as it descends it is still smaller than the corresponding osmolarity in the ISF

What is happening to the reabsorption of Na+, Cl-, and other ions in the descending loop of Henle?

No reabsorption is occurring

What is moving out of the lumen in the ascending loop of Henle and why?

The solutes are leaving to maintain the osmolarity in the ISF.

If water is exiting from the lumen of the descending limb to try and balance the osmolarity, why does it not stabilize and keep moving out?

Even though water is moving out it is still bigger outside than inside, which causes water to keep flowing down its gradient to the ISF.

When is the osmolarity between the ISF and the loop of Henle at equilibrium?

at the bottom of the loop

What happens to the osmolarity in the ascending loop of Henle?

It decreases as it goes up

Why is water not exiting in the ascending loop of Henle?

There are no aquaporins

In the ascending loop of Henle, what gets Na+, K+, and Cl- across the luminal membrane?

The NKCC carrier takes 1K+ and 2Cl- across the membrane along Na+ gradient

What are the ways that Na+ gets taken out of the lumen in the ascending loop of Henle?

NKCC carrier (luminal membrane), sodium channel (luminal membrane), and Na/K pump (basolateral membrane)

What happens to Cl- once it gets through the luminal membrane in the ascending loop of Henle?

It exits via Cl- channels across the basolateral membrane.

What happens to K+ after it has crossed the luminal membrane in the ascending loop of Henle?

It exits through potassium channels on the basolateral membrane.

In the loop of Henle, what gets reabsorbed more the solute or water? How do you know?

More solute is reabsorbed in the ascending loop of Henle. This is determined because the change in osmolarity is greater in the ascending loop than the descending loop and it ends with a lower osmolarity meaning more solutes were absorbed

What is the osmolarity at the start and end of the distal tubule?

100mOsm at the start and 300mOsm at the end

If water is exiting the descending limb in the loop of Henle, why is the hydrostatic pressure not building up in the ISF?

Water gets uptake by the peritubular capillaries

What are the different aquaporins in the cells on the collecting tubule and where are they located?

Aquaporin 3 and 4 (always open)- located on basolateral membrane

Aquaporin 2- located on luminal membrane or vesicle inside cell

What direction does water go from the medullary collecting tubule and why?

If aquaporin 2 is open on the luminal membrane, water flows out of the lumen and eventually is pushed into the ISF

What are the two locations of aquaporin 2, and when are they there?

Aquaporin 2 is either located on the luminal membrane or on a vesicle inside the nephron epithelial cell. During dehydration, it is located on the luminal membrane. When not dehydrated, it is located on a vesicle inside the cell.

Without aquaporin 2 on the luminal membrane of the medullary collecting tubule, can Na+ and Cl- still be reabsorbed, if so how?

Yes, they go through channels on the luminal membrane. Na+ is then pushed across the basolateral membrane via the Na+/K+ pump and Cl- goes through a channel on the basolateral membrane.

What determines the osmolarity in urine?

The location of aquaporin 2

If there are no aquaporin 2 channels on the luminal membrane, what happens to the osmolarity?

It is decreased

What hormone regulates aquaporin 2 location?

Anti-diuretic Hormone (ADH)

What is the other name for ADH?

Vasopressin

How does ADH affect urine osmolarity and aquaporin 2?

If ADH is present, aquaporin 2 is located on the luminal membrane which allows water to exit the lumen causing the osmolarity to increase.

What can cause ADH to be produced?

Dehydration

How does ADH directly affect aquaporins?

ADH binds to a receptor on the basolateral membrane of the nephron cell on the collecting tubule. This activates the alpha protein (Gs protein) which turns on adenylyl cyclase and generates a cAMP. This then turns on a protein kinase that phosphorylates the fusion protein located on the vesicle containing aquaporin 2. This fusion protein the combines with the one located on the luminal membrane, causing exocytosis and allowing aquaporin 2 to be transferred to the luminal membrane.

Where does ADH come from?

The posterior pituitary gland

How is K+ flow different in the collecting duct?

K+ is going into the lumen instead of out

What are the two factors that can lead to an increase in ADH?

Dehydration and Low Blood Pressure

How do high levels of ADH lead to a decrease in urine volume?

It creates a high number of aquaporins on the luminal membrane of the nephron cells in the medullary collecting tubule which leads to an increase reabsorption of water which decreases urine volume and increases the osmolarity of the urine.

Of the neurons that produce ADH, where are the cell body and axon terminal located?

The cell body is in the hypothalamus and the axon terminal is located in the posterior pituitary gland

From the axon terminal, where is ADH released to and where does it eventually end?

ADH is released into the blood where it will go to the kidneys and arterioles.

What can cause dehdyration?

Sweating

What is the osmolarity of sweat and how does it affect the solute concentration in the ECF?

100mOsm. Since it is high in water that means the ECF has an increased solute concentration making it hyperosmotic.

How and why does the osmolarity of sweat go from 300mOsm in the sweat gland to being released as 100mOsm?

At the bottom of the sweat gland, water, Na+, and Cl- enter creating an increased concentration of solute, however, as it goes up the channels located on the cell surrounding the lumen only are for Na+ and Cl-. This keeps water in the lumen while solutes exit, decreasing the osmolarity.

During sweating, what happens to the neuron size and why?

The amount of volume is decreased causing the cell to shrink. This is because the solute concentration of the ECF is increased during sweating which creates a gradient for water that favors efflux, as inside is 300mOsm.

Why is sodium entering the dendrite of a neuron containing ADH, and what does it cause?

Since there is a build up of sodium and other solutes in the ECF, it binds to the dendrite which causes an action potential that makes its way to the axon terminal causing ADH to be released.

How does an action potential affect the volume and [solute] in the kidney/arteriole?

The action potential causes ADH to be released into the blood where it goes to the kidneys and arterioles. Here the volume decreases and the concentration of solute increases

How does a decrease in blood pressure lead to the release of ADH/vasopressin?

Neurons associated with baroreceptors with a low amount of action potentials synapse in the medulla (CV center) here an inhibitory neuron acts which increases the action potentials along this axon, that then synapses in the hypothalamus with a neuron that can release ADH. This then causes action potentials to fire down the axon and ADH is released from the axon terminal.

How does alcohol lead to an increase in urine production?

alcohol slows neurons down which thus causes ADH release to decreasing and increases urination.

What is Diabetes Insipidus?

It is when there is a decrease in ADH production which causes a large increase in urine output.

Where does potassium secretion occur?

The lumen of the distal tubule or cortical collecting tubule

How does the potassium secretion occur/ what channels lead to this?

On the basolateral membrane of the nephron epithelial cell (D.T. or C.C.T.) the Na+/K+ pump is pushing Na+ out while pumping K+ in. However, there are very few K+ channels open on the basolateral membrane so it cannot go back out. There are also many K+ channels located on the luminal membrane, so while Na+ and Cl- are pumped out of the lumen, the K+ goes through those channels into the lumen where it can get secreted.

What hormone regulates K+ secretion?

Aldosterone (steroid)

What does aldosterone do once inside the nephron cell?

It binds to a receptor that then allows it to act as a transcription factor that then goes to the nuclease and activates genes and turns them into mRNA.

In the nephron epithelial cell (D.T. or C.T.T.) how does mRNA affect sodium movement?

It increases the number of sodium channels and Na/K pumps.

How does aldosterone ultimately increase K+ secretion?

Aldosterone ultimately produces mRNA within the cell which increases the Na+ channels and Na/K pump, pumping more Na consequently putting more K inside the lumen.

What is the different in the distal tubule compared to the other parts of the collecting duct?

The potassium channels are located on the luminal membrane and allow potassium to be secreted

Where does aldosterone come from?

The epithelial cells in the adrenal cortex

Why can aldosterone go through the basement and basolateral membrane easily?

It is very lipid soluble

What happens when proteins (Na channel and pump) are activated by aldosterone?

Sodium permeability is increased and sodium exit increases

How does aldosterone effect urine output?

It decreases the loss in urine, specifically the loss of water, Cl-, and Na+ and increases K+ excretion in the urine.

What two things regulate of aldosterone production?

1) Increased K+ in the ECF of the body

2) Juxtaglomerular apparatus

What is contained within the juxtaglomerular apparatus?

Distal Tubule Cells and Endothelial Afferent arterioles

How does increased K+ in the ECF increase aldosterone production?

It interacts with the epithelial cells of the adrenal cortex which is where aldosterone is made

What are the ways that decreased sodium in the distal tubule cell can impact aldosterone?

Decreased sodium can lead to the production of renin which will make angiotensin 2 that can eventually make aldosterone or it can activate a paracrine which activates the endothelial afferent arterioles and produces renin.

In addition to low sodium what is another signal that can lead to increased aldosterone production?

Low blood pressure in the endothelial afferent arterioles leads to the production of renin which makes angiotensin 2 that can make aldosterone.

How are arterioles, capillaries, and venules arranged and what direction does the blood flow?

Arterioles → capillaries → venule

Blood enters the arteriole then goes through the capillary and venule.

What sits inside the capillary?

Endothelial cells sit on the basement membrane of the capillary

What is outside the capillary?

ISF and cells that take up excreted solutes or gives off solutes that get taken up by the capillary

What do red blood cells provide?

oxygen

What is flowing through the capillaries and leaving?

Fatty acids, RBC, glucose, and water

What is entering the capillaries?

C02, NH3, and water

How does water, fatty acids, glucose, carbon dioxide, NH3, and red blood cells get in and out of the capillary?

Free diffusion

When does free diffusion work well?

When the capillaries and cells are close together