Renal Flashcards Preview

Physio Test 2 > Renal > Flashcards

Flashcards in Renal Deck (88):

What are the 4 main functions of the kidney?

1. It's a homeostatic organ that mainly works to control electrolyte/mineral/body fluid content via the production of urine

2. Excretes waste products via urine

3. Endocrine organ that secretes calcitriol (calcium production), EPO (RBC production), and renin (BP control)

4. Acid/Base modulator


Whats the indicator dilution method? Function?

It's used to find the volume of a body fluid

You inject a known quantity of a substance into the body that latches onto a specific bodily fluid...then after it has equilibrated in the body, you remove blood sample and measure concentration in plasma sample

use C= Q/V to find the volume

ex: radioactively labeled RBCs for polycethemia diagnosis


What is hematocrit?

It's the number of RBCs in the blood


Whats the major source of intake and output?

Intake = Drinking
Output = Urination


What's the main regulator of volume in the body? Regulator of osmolarity?

Volume = Sodium content (higher Na = hypervolemia & lower Na = hypovolemia)...this is why sodium sensors in the body tend to be pressure sensors...HOW RENIN-ANGIOTENSIN WORKS

Osmolarity = Water content (higher water = hyposmosis & lower water = hyperosmosis)...this why water sensors are primarily osmosensors...HOW VASOPRESSIN WORKS


What is the importance of inulin and paraminihippuric acid? What can they help to estimate?

Inulin: Doesn't get reabsorbed or secreted so it's a good measure of GFR

PAH: Gets completely secreted and thus can be a good estimate of RPF


Describe the tripartite filtration barrier? (Layers, different components and the stuff

the capillary endothelial cells have large openings called fenestra that allow for particles to pass through...then you have the thick basal lamina (basement membrane). Outside of this you have the podocytes which have processes that attach to the outside of the basement membrane

B/w the podocyte processes, you have large filtration slits that are covered by extracellular matrix materials and the slit diaphragm...this provides further filtration on top of the filtration slits


What is the filtrate that comes out of the glomerulus missing from the normal plasma?

PROTEINS are NOT allowed to pass through the fenestrated openings of the capillaries and also through the filtration slits


What is the primary factor by which the glomerulus filters? secondary factor?

1st is size so bigger don't get in (AKA proteins)
2nd is charge (neutral or positive is perfect)


What are the size limits for a molecule being filtered? When does charge play a role?

If it's s between 4-8 nm then charge comes into play and partially filtered...note that the filtration slit is negatively charged and thus they repel negatively charged proteins and attract positively


What can be one reason for early albuminuria in the urine

If you albumin lose their negative charge, then they'll pass through the filtration slits more easily and thus be found in the urine at higher concentrations than normal


Describe the process of using creatinine? What does it help you assess/measure?

Creatinine is a by product of muscle metabolism and is found in produced at nearly a constant rate

Thus, you can normally use it to measure GFR. People tend to just look at the creatinine level in the blood and see if it's low (Higher than normal GFR) or high (Lower than normal GFR)


Why can creatinine be a flawed means of measuring GFR?

B/c it is also secreted to a certain extent. Thus, the actual plasma concentrations will be lower than normal

Also, creatinine is a good predictor when you have really low GFR and a poor predictor at high GFR...therefore it can be a good indicator but only when you're in really deep shit


What is cystatin C and what can it be used to measure?

This can be used to assess GFR and is much better than creatinine

HOWEVER, you can't use it for clearance since it is fully broken down in the nephron tubules


What are the two factors that affect GFR? Go in depth

1. Starling Forces determine the level of if you have more hydrostatic pressure in the glomerular capillaries then you will be favoring filtration. But if you increase the oncotic pressure of the glomerular capillaries, increase the hydrostatic pressure in the bowman's capsule, or decrease the hydrostatic pressure in the glomerular capillaries, then you will favor reabsorption. MAJOR DRIVING FORCE IS THE HYDROSTATIC PRESSURE IN GLOMERULAR CAPILLARY

2. RPF. if you increase RPF, then you decrease the likelihood of reaching filtration equilibrium b/c you've also increased the pressure inside the glomerular capillary. If you decrease RPF, then you increase the chance of reaching filtration equilibrium before the capillary is done and thus create areas of wasted capillary.


What is filtration equilibrium?

This is the point where you no longer undergo filtration b/c the oncotic pressure in the glomerular capillary = hydrostatic pressure in the capillary...can happen if you continue to concentrate the blood by undergoing filtration or if you decrease the pressure of the blood flowing through the capillary


What are the conditions of FF, GFR, and RPF at filtration equilibrium?

At filtration equilibrium, the FF is constant and GFR is direction proportion to RPF

As, RPF increases FF decreases b/c while GFR increases it does so at a much slower rate


What are the two factors that allow for increased reabsorption in the peritubular capillaries?

1. The pressure in the peritubular capillaries is super low b/c it has dropped once in afferent arterioles before enter the glomerular capillary and again in the efferent arteriole

2. The blood has been soo thoroughly filtered that it is mostly made up of proteins and has a very high colloid oncotic pressure at that point


How is glomerular capillary pressure mainly controlled?

Via afferent arteriole vasoconstriction b/c this reduces both Pressure and RPF

The efferent only vasoconstriction actually increases pressure initially before the reduced RPF kicks into effect and causes the pressure to drop

Vasoconstricting both causes a reduction in RPF but also an increase in the pressure


What is autoregulation? What are the two ways in which it is controlled?

Autoregulation is when you hold your GFR and your RPF at a constant level over a certain range of blood pressure (90-160 mm Hg)

1. Myogenic response...stretch activating calcium channels open up...vasoconstricts the afferent arterioles

2. Macula densa senses flow in the afferent arteriole when the DCT touches it. If the flow is high, then it increases delivery of NaCl to the macula dena. This causes secretion of adenine from the macula densa into the afferent arteriole. This adenine secretion vasoconstricts the afferent arteriole and reduces the


Describe the Renin-Angiotensin system effects in autoregulation

Major effect: Increase salt reabsorption through aldosterone release. Also, produces angiotensin II that constricts both the efferent and afferent arterioles. This reduces the GFR slightly and severely decreases the RPF. Also, greatly increases the FF, which increases the oncotic pressure in the pretubular capillaries (due to high protein content)...this promotes reabsorption!!!!

Reduces surface area for filtration and decreases the Kf and thus the rate of filtration


Describe the effects of the sympathetic nervous system in autoregulation

As BP decreases, baroreceptors in the carotid and aortic arches fire slowly and trigger the SNS to constrict afferent and efferent arterioles. This decreases RPF, increases FF, and increases oncotic pressure in peritubular capillaries

Also causes secretion of renin and production of angiotensin II


Describe the effects of the ANP and Prostaglandins

- opposes renin-angiotensin system and is secreted by atrial myocytes when it stretches due to increased BP in the body
- Vasodilator that acts on both AFFERENT & EFFERENT ARTERIOLES to increase GFR and thus increase Na excretion
- Inhibits aldosterone & renin secretion

- Vasodilators made in the kidney in response to angiotensin II & increased sympathetic activity
- Helps to limit its effects and turn it off


Whats the difference b/w a moderate and maximal sympathetic activity?

Moderate: causes a small decrease in GFR and helps sodium reabsoprtion

Maximal: favors constriction of the afferent arteriole (NOT BOTH) and thus reduces GFR by a lot as well and almost shuts down the kidney...this is what people in shock have when they lose a lot of blood...stop filtrating the blood well


Why can NSAIDS damage the kidney when renal perfusion is low?

NSAIDs stop the synthesis of prostaglandins that act as a brake to prevent over vasoconstriction in response to low renal perfusion

Thus you reduce the blood flow even more and cause more renal damage


What are the two main mechanisms for Na reabsorption from the tubular lumen into the interstitial fluid?

1. Transcellular. You transport Na into the cell from the tubule via an apical channel/carrier. Then you move the Na out of the cell through the basolateral side via the Na/K ATPase...this is also the one that's affected by diuretics
2.Paracellular: moves through the tight junctions b/w cells due to a tubular electrochemical gradient


What are the mechanisms used to reabsorb Na from the early PCT?

1. Na/H antiport where H is secreted per Na reabsorbed. This proton in the lumen combines with a bicarbonate and forms carbonic acid that breaks down into water and CO2. The CO2 enters the cell again and combines with water to form carbonic acid, which is broken down into bicarbonate ion and a proton by CARBONIC ANHYDRASE. the proton then goes and brings in another Na. Meanwhile, the water from before, goes paracellular into interstitial fluid.

2. You have a Na/Glucose cotransporter


What are the mechanisms used to reabsorb Na from the late PCT?

1. you have two antiporters that bring in Na and Cl while kicking out H+ and an anion, respectively. in the lumen, the H+ and the anion combine together and enter the cell, where they dissociate again and bring back another Na and Cl

2. The Cl- gradient favors movement of Cl- from lumen to interstitial fluid. This causes the areas locally around the transporter to be positive. This positive charge is the driving force for the paracellular transport of Na


Why is there a net negative charge in the lumen at the end of the PCT? And what is the osmolarity of the tubular filtrate after re-absorption of Na in PCT?

From the two mechanisms in the early PCT (1. Na/H antiport 2. Na/Glucose cotransport) that bring in Na but leave Cl- in the lumen, causing a negative charge

After the PCT, it goes from hyperosmotic to isosmotic


What ions are mainly reabsorbed by the PCT?

Na and HCO3-


What is the mechanism for reabsorbing Na in the tall ascending loop section?

You have a Na/K/2Cl transporter that actively brings in all 3 ions into the cell. Then the K is released back into the lumen to be recycled and ensure that this transport can continually happen.

This also creates a net positive charge in the TAL segment, which leads to the paracellular expulsion of Na/K/Mg/Ca from the lumen into the interstitial fluid


What is the mechanism for reabsorbing Na in the early DCT? Late DCT/Collecting duct?

Early DCT --> Na/Cl cotransport

Late DCT/CD ---> you have an eNaC channel that allows for Na to flow inside the cell. The lack of Cl- coming out causes a huge negative charge in the lumen, which acts as the electrochemical graident for moving Cl- out paracellularly. Also, you have a channel that releases K into the lumen to ensure you still have an electrically negative cell that allows for the Na to move in.


What is thiazaide? furosemide? acetazolamide? amiloride?

Thiazide block the Na/Cl cotransporter in early DCT

Furosemide blocks the Na/2Cl/K in TAL

Acetazolamide blocks the Carbonic anhydrase in the early PCT and stop Na reabsorption by reducing the supply of H+ in the cell that can be sent out

Amiloride blocks the eNaC channel in the end and is known as a K-sparing diuretic


What is effective circulating volume?

It's a measure of the efficiency of tissue perfusion by blood...HOW WELL DOES BLOOD CIRCULATE TO THE TISSUES IN THE BODY


What regulates ECV? How does it do this?

Baroreceptors help to regulate ECV.

Baroreceptors in the juxtaglomerular apparatus affect renin secretion

Low pressure sensors in the pulmonary vein & atria that regulation secretion of ANP

High pressure sensors in the carotid sinus & aortic arch that regulate sympathetic activity


What's the difference b/w short term and long term homeostatic volemic effectors?

Short term CHANGE BP by affecting heart and blood vessels

Long term CHANGE SODIUM EXCRETION by affecting the kidneys


What are two hemodyamic effects on the regulation of Na reabsorption?

1. Increased RPF and GFR will cause increased Na excretion

2. Starling forces at the peritubular capillaries. If you have low hydrostatic pressure or high oncotic pressure, then you favor reabsorption


What is back flux?

This is when you favor filtration in the peritubular capillaries, and thus any reabsorbed material in the interstitial fluid goes back into the tubule


What stimulates/inhibits the renin-angiotensin aldosterone system (RAS)? What does RAS control?

Stimulated by LOW BP, sympathetic stimulation, & reduced delivery of NaCl to the macula densa

Inhibited by High BP, ANP, and increased delivery of NaCl to the macula densa

RAS controls the reabsorption of Na and thus the blood volume


Describe the formation of angiotensin II. What are the 3 inhibitors?

Angiotensinogen by the liver is modified by renin by the kidneys into angiotensin I. This is further cleaved by ACE into angiotensin II.

Aliskiren (Tecturna) is a renin inhibitor. Captopril is an ACE inhibitor. Losartan is a AT1 receptor antagonist.


Why is captopril worse than losartan?

While both help to reduce BP by affecting the effect of Angiotensin II. Captopril is an ACE inhibitor w/ side effects that are due to ACE's secondary function of degrading bradykinin into its metabolic factors. If ACE is inhibited, then bradykinin builds up and causes vasoconstriction & coughing.


What are the effects of angiotensin II?

RESISTANCE: Increases resistance in afferent and efferent arterioles that increases FF and reduces RPF. This increases oncotic pressure and decreases hydrostatic pressure in peritubular capillaries. Stimulates reabsorption of Na
EXCHANGER: stimulates the Na/H exchanger in early PCT and the eNaC channel in the late DCT/collecting tubule


Why can renal stenosis cause hypertension?

This reduces the RPF to the kidney and makes them think that you have reduced blood volume...hence increases renin secretion and increases blood volume...leads to hypertension


What are the effects of aldosterone?

Increases the transcription of Na/K ATPases and eNaC channels to increase Na reabsorption in the collecting duct and DCT

Also, increases K+ secretion


What's the effect of Sympathetic nervous activity?

Constricts afferent and efferent arterioles that leads to increased re-absorption in peritubular capillaries

Increases renin secretion

Stimulates Na/H antiport & Na/K ATPase in PCT to increase Na reabsorption


What's the effect of ADH/vasopressin?

1. Increases free-water reabsorption in the collecting tubules (

2. Increases the activity of Na/K/2Cl transporter in TAL

3. Increases activity of eNaC in the DCT


What's the effect of spironolactone?

This is an aldosterone antagonist!


How do you differentiate b/w low perfusion or acute tubular necrosis being the reason for acute renal failure?

Low perfusion based ARF is due to a fractional excretion below 1%

Tubular necrosis causes fractional excretion to be higher than 2%


What is primary & secondary hyperaldosteronism (Plasma Na, BP, Plasma K, Blood pH, and Renin)?

This is an abnormally large increase in your aldosterone due to increased secretion by the adrenal medulla. it causes your plasma Na to remain unchanged (water also brought in to balance this out), BP to be increased, K excretion increases and decreases plasma K, blood pH becomes more basic, and renin concentrations decrease (negative feedback)

secondary is similar to primary in terms of symptoms..instead you have a known cause (usually due to increased renin-angiotensin II)


What are two causes of secondary hyperaldosteronism?

1. Renal artery stenosis
2. Hypovolemia


What is bartter syndrome (4 types, plasma K, urine volume, ECF volume, plasma aldosterone, blood pH, urinary Ca/Mg excretion)?

This is a defect in the transporters of the TAL.
Type 1 is a defect in the Na/K/2Cl. Type 2 is a defect in the apical K channel. Type 3 is a defect in the basolateral Cl channel. Type 4 is a defect in the barttin subunit of the basolateral Cl channel

Plasma K decrease, Urine volume increases, ECF volume decreases, plasma aldosterone increases, blood pH increases/basic, urinary Ca/Mg excretion increases


What is Gitelman syndrome (urine volume, ECF volume, plasma K, plasma aldosterone, blood pH, urinary Ca excretion)?

Defect in the Na/Cl cotransporter in the early DCT and is less severe than barrter syndrome since the DCT only accounts for 7 percent of the Na reabsorption

urine volume increases, ECF volume decreases, plasma K decreases due to increased plasma aldosterone, blood pH increases (basic), urinary Ca excretion decreases


What is Liddle syndrome (Na reabsorption, ECF volume, Plasma K, Plasma aldosterone)? Treatment?

Defect in the eNaC that hyperactivates. Na reabsorption increases, ECF volume increases, Plasma K decreases, and Plasma aldosterone decreases

Treatment: Amiloride which inhibits the eNaC


What is psedohypoaldosteronism (ECF volume, BP, Plasma K, Aldosterone)?

This is a defect in the eNaC channels that inactivates them or in the aldosterone receptor that prevents it from recognizing the hormone. Causes hypoaldosterone like symptoms even though you'll have high levels of aldosterone

ECF volume decreases, BP decreases, plasma K increases, and ALDOSTERONE INCREASES


What is central diabetes insipidus (urine volume, urine osmolarity, plasma Na)? Treatment?

This is when you have no ADH and this causes increases urine volume, reduce urine osmolarity, and increased plama Na since you don't have as much water coming back into the cell

Treatment: GIVE THEM ADH


What is nephrogenic diabetes insipidus? Treatment?

Similar symptoms to CDI however, the reason for this is due to LACK OF ADH RECEPTOR or LACK OF AQUAPORIN

Treatment: Reduce sodium intake and drink plenty of fluids...can't give them ADH since that won't do anything


What is diabetes mellitus (osmotic diuresis)? Urine volume, Na excretion, K excretion, and ECF volume?

This is a condition where you have increased water in the collecting tubules and they can't be taken out. Urine volume increases, Na & K excretion increases b/c increased water in the tubule reduces their concentrations and thus their driving force to move into interstitium, and ECF volume decreases

Treatment: Provide patient w/ insulin and fluids with Na & K


What are phlorizin and canagliflozin? What's the difference?

These are both SGLT inhibitors that are used in diabetes to prevent the reabsorption of glucose

Canagliflozin can also cause dehydration by affecting the uptake of sodium and thus reducing the water intake as well


What is the threshold of glucose reabsorption and what happens when you surpass it?

Glucose reabsorption threshold = 200 mg/dl

if you go above this value then you will start to see glucose in your urine b/c of the over saturation of SGLT transporters...thus your clearance is not enough


What is Splay?

this is the gradual approach to Tm at high plasma glucose levels


When are amino acids and carboxylates reabsorbed?

Both are essentially completely reabsorbed by the end of PCT

AA: antiport with H
Carboxylates: cotransported w/ Na


Why is the concentration of K important?

K+ is the most permeable ion in the cell and it therefore dictates the membrane voltage...having too much K in the extracellular matrix causes depolarization of the membrane and makes you more excitable since you have a more positive voltage than normal due to reduce driving force. Meanwhile, decreasing extracellular K causes hyperpolarization as a large amount of K leave the cell


Why is the concentration of K important?

K+ is the most permeable ion in the cell and it therefore dictates the membrane voltage...having too much K in the extracellular matrix causes depolarization of the membrane and makes you more excitable since you have a more positive voltage than normal due to reduce driving force. Meanwhile, decreasing extracellular K causes hyperpolarization as a large amount of K leave the cell


What are the two ways to control plasma concentrations of K?

1. Rapid Method: Where the cells simply take up the k and act as a buffering mechanism

2. Slower method: Increased excretion by kidneys


How does the slower K renal excretion work? Also describe the secretion portion?

95% of filtered K is reabsorbed (65% in PCT via paracellular transport; 30% in PCT via Na/K/2Cl and paracellular transport; type A intercalated cells very minor amounts)

Secretion (small amount): increased plasma [K+] causes an increase Na/K ATPase activity that increases the K uptake by intercalated cells from the interstitium --> increases secretion (usually this is used to push out reabsorbed Na into the interstitium). Also, high tubular Na causes increased Na reabsorption and this leads to increased K secretion . FINALLY HIGH FLOW RATE INCREASES K SECRETION


Why do loop diuretics like furosemide and thyazide cause increased loss of K? What do amiloride and spironolactone do to K?

F & T = increase the flow rate and thus cause loss of K

A & S = retain K (AKA K-sparing)


Why does hypokalemia lead to increase in blood pH? hyperkalemia ---> acidosis?

Cells have a K/H antiport where K exits the cell and H+ enters the cell. When you have hypokalemia, this works in overdrive to restore plasma [K] and in doing so you pull out a lot of protons making it basic

Hyperkalemia, you have reduced function of this mechanism and this causes H+ to not be pushed into the cell and rather it collects on the outside


Why can hypocalcemia cause you to be hyperreflexia and more excitable?

If you decrease calcium extracellularly, then you need smaller and smaller depolarization to activate the Na b/c you depolarize the membrane

Thus, with hypocalcemia you can more easily excite the Na ion channels to activate and form an AP


Why can hypocalcemia cause you to be hyperreflexia and more excitable?

If you decrease calcium extracellularly, then you need smaller and smaller depolarization to activate the Na b/c you depolarize the membrane

Thus, with hypocalcemia you can more easily excite the Na ion channels to activate and form an AP


Describe Ca reabsorption. What does PTH regulate?

65% of this happens in PCT and is paracellularly. Another 25% occurs at the TAL paracellularly along w/ Mg, Na, & K. Finally, at the DCT 8% reabsorption that is mostly transcellular via plasma membrane Ca ATPase & Na/Ca exchanger

PTH regulates reabsorption by the TAL & DCT


What is primary hyperthyroidism?

You have too much PTH and thus you have high Ca and low phosphate in plasma

High Urine [Ca]

Can cause bone problems and kidney stones


What happens when you have high urine calcium concentrations in primary hyperthyroidism?

If this is happening due to increased plasma Ca, then you have a Ca sensing receptor in the tubular cells that directly inhibits the Ca reabsorption



What's the function of the Calcium Sensing receptor (CaSR)?

It senses the levels and sends the signal to the parathyroid gland, which regulates PTH secretion

Can be in the basolateral membrane of tubular cells

If you have low plasma Ca, then it increases reabsorption, increases formation of vitamin D3 (HIGHER PTH)

If you have high Ca, then decreases PTH secretion and inhibits reabsorption


What is Familial hypocalciuric hypercalcemia (FHH)?

A mutation that makes the CaSR to always act as if the plasma [Ca] is low...thus continually high PTH, Ca reabsorption, plasma [Ca]

HOWEVER, you will have low urine [Ca]


What is Familial hypocalciuric hypercalcemia (FHH)?

A mutation that makes the CaSR to always act as if the plasma [Ca] is low...thus continually high PTH, Ca reabsorption, plasma [Ca]

HOWEVER, you will have low urine [Ca]


What's the effect of loop diruetics, thiazide, amiloride on Ca?

Loop diuretics (furosemide): Inhibit the transporters in the TAL and thus reduce the positive charge gradient in the tubular lumen. Causes a reduction in the Ca reaborption paracellularly

Thiazide: inhibit Na/Cl cotransporters in early DCT and this causes less Cl- in the cell which hyperpolarizes the cell ---> This increases the driving force for Ca to enter the cell --> increases Ca reabsorption

Amiloride: inhibits the eNaC channel in late DCT and increases the driving force for Ca to enter the cell ---> increases Ca reabsorption


What two mechanisms are used to eliminate drugs and foreign substances?

filtration with little reabsorption


What are the secretion mechanisms for drugs at the proximal tubule using an anion antiporter?

The cell has Na-K-ATPase which creates the Na gradient. This sodium gradient is used to drive alpha keto gluterate into the cell. The AKG is then expelled into the blood and the anion (PAH) enters. PAH exits the cell into the lumen via an unknown mechanism.


What are the secretion mechanisms for drugs at the proximal tubule using a cation antiporter?

Na/K/ATPase creates a concentration gradient and the cation enters the cell via facilitated diffusion. H+ and the cation (excreted) are exchanged at the luminal membrane and using the Na gradient, Na is brought in and H+ is expelled.


Why is cAMP found in the urine in primary hyperparathyroidism?

PTH increases cAMP production (receptor --> AC --> cAMP). It is found in the urine because of the anion antiporter starts moving it into the lumen because there is too much of it.


What is the use of PAH? and Glucuronides?

PAH is used to measure RRF. Glucuronides help the kidney excrete H2O soluble substances


Why do we sometimes give probenecid with penicillin?

We give probenicid with penicillin because probenecid will be removed by the same transporter as pencillin. Therefore, penicillin will be able to the stay in the body longer.


Describe HCO3 transport at the proximal tubule where 80% is reabsorbed. How does the TAL differ?

HCO3 in the proximal tubule: The luminal membrane has a Na/H exchanger. As you reabsorb Na, H is excreted. It combines with HCO3 in the lumen and forms H2CO3 using carbonic anhydrase. This is broken down into H2O and CO2 and moves back into the cell. There, it uses carbonic anhydrase to go back to H+ and HCO3. H+ is used in the Na/H exchanger again and HCO3 is reabsorbed in the blood using HCO3/ Cl- exchanger or Na/HCO3 cotransporter

TAL differs because it has proton pumps.


How do alpha intercalated cells handle HCO3? What about beta?

Alpha cells reabsorb another 10% of filtered load of HCO3 so almost all filtered HCO3 is reabsorbed. It uses two different mechanisms: H-ATPase and H-K ATPase (which is the source of K+ reabsorption in the cell). For each H+ that is secreted, one HCO3 is synthesized and reabsorbed.

Beta cells secrete HCO3. Organized in the opposite way of alpha cells.


What are the two ways of secreting H+? Describe them.

One way is via titratable acids and the other way is through NH4+.

Titratable acids: Done via the alpha intercalated cells. The H+ that is secreted combines with buffers in the blood (PO4, urate, lactate, etc).

NH4: In the proximal tubule, glutamine is broken down into the NH3 and glucose. NH3 combines with H to make NH4. This is secreted into the urine via the Na/H exchanger. Glucose goes on to make CO2 and H2O which gives rise to HCO3. Na-HCO3 cotransporter allows the HCO3 to go back into the blood.

Remember glutamine transport into the cells is regulated. It increases when plasma pH falls.


Describe the action of carbonic anhydrase inhibitors, amiloride, thiazides and furosemid.

carbonic anhydrase inhibitors: inhibits HCO3 reabsorption so alkanize the urine

amiloride: inhibit ENaC which makes the lumen more positive and reduces the driving force for H+ into the lumen. Alkanize the urine.

Thiazides and furosemide: works on Na/K/2Cl and Na/Cl cotransporters.
Causes volume contraction -->RAS--> Aldosterone--> secrete H+
Enhance Na+ delivery to collecting tubules --> ENaC activity increased --> lumen more negative --> H+ pump increases and more H+ secretion

K+ wasting --> hypokalemia --> more H+ into tubular cells --> H+ secretion


Describe the process of micturition.

The detrusor muscle is innervated by parasympathetic nerves and the internal sphincter is innervated by sympathetic nerves. The external sphincter is innervated by somatic nerves.
Somatic sensory nerves detect wall stretching and the urge to urinate begins. Pontine centers inhibit the detrusor and keep spinchters closed to prevent urination.

When you relax your external spinchter, the pontine centers stop inhibiting parasympathetic nerves to detrusor.


What are the endocrine functions of the kidney?

1. Renin Angiotensin System
2. Calcitrol (1,25 diOH vitamin D3): It is made in the liver and the kidneys activate it. The main function is the increase Ca2+ absorption in the intestines. If you have kidney failure, it might cause bone problems. A lack of Vitamin D causes rickets.
3. Erythropoietin: It is made in the kidney and induces the formation of RBCs. Patient in kidney failure are usually anemic.