Mech of Disease Renal Disease
Terms
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- what are the 4 main functions of the kidney/nephron?
- 1. reabsorb filtered nutrients 2. tubular secretion 3. eliminate/conserve H20 4. adjust plasma pH
- Where does reabsorption take place?
- proximal tubule
- What are things that get reabsorbed?
- Vitamins, glucose, minerals, amino acids
- Where does secretion take place
- in the renal tubular cells
- what gets secreted
- drugs/toxins
- How does secretion take place?
- via secretory/transport mechanisms in the tubular cells
- how do the mechanisms work
- tubular cells grab the substance from the peritubular capillaries and actively secrete them into the tubular fluid
- Do drugs get filtered into the urine on their own
- no- usually bind to plasma proteins like albumin
- How is urine osmolality adjusted?
- by eliminating or conserving H20
- When the body is H20 deprived, what happens to osmolality?
- increases: very concentrated urine (1200 milliosmoles/liter)
- When there's too much water what happens?
- decreases osmolality: urine contains more water
- How is plasma pH adjusted?
-
by secreting H+ ions and making and conserving
bicarbonate ions - What's the normal pH in the plasma?
- 7.4
- whats the NL [Na+] in plasma?
- 0.14 M
- What causes many problems with the acid/base balance?
- sulfuric acid breakdown
- When acid/base problems arise, what do the kidneys do?
- adjust the H+/HCO3- ions
- When acid/base problems arise, what do the lungs do?
- adjust by ventilating more or less
- What hormone does the kidney secrete to produce RBC's
- erythropoetin
- What is another hormone the kidney produces?
- renin
- What does renin do?
- end result= BP inc'd
- What does aldosterone do?
- inc's Na+ reabsorption in renal tubules and increases K and H+ secretion into tubular fluid.
- What does the kidney have to do with Vitamin D?
- it converts 25-OH Vitamin D (inactive form) to 1.25 (OH)2 Vitamin D (the active form)
- What is the significance of this conversion?
- 1. increases Ca2+ absorption in the gut 2. assimilates dietary stuff into blood
- What effect does parathyroid hormone have on the kidney?
- causes increased Ca2+ reabsorption from tubular fluid; causes osteoclastic activity
- When is it secreted?
- decreased Ca2+ in plasma
- What secretes ADH (vasopressin)?
- posterior pituitary
- What affect does ADH have on kidneys
- when osmolality is too high (you get dehydrated) it causes kidney to increase H2O reabsorption in collecting ducts
- What is the proportion of plasma to cells in blood flowing into the kidney?
- 55% plasma, 45% cells
- trace the bloodflow thru the kidneys
- afferent artery -> glomerular capillaries -> efferent artery -> peritubular capillaries
- What is the structure of glomerular capillaries?
- single fenestrated layer of endothelial cells on top of a basement membrane and foot processes of visceral podocytes
- What features easily allow movement in and out
- single layered and fenestrations
- contractile, phagocytic cells that respond to complement cascade by secreting chemical junk; also secrete a matrix
- mesangial cells
- describe glomerular filtration barrier
- triple layer of glomerulus with a negative charge
- significance of neg charge?
- keeps neg charged particles out of urine like albumin
- definition of GFR
- the amount of plasma filtered out of the capillaries into bowman's space
- quantify the rate at which plasma is filtered
- amt excreted = amt. filtered + amt. secreted - amt. reabsorbed
- What was the basis for the inulin experiment?
- inulin is neither secreted nor reabsorbed and is freely filtered; therefore the amt filtered = the amt excreted
- What was the avg GFR determined to be?
- 125 mL of plasma/minute
- does all plasma go thru glomeruli?
- no
- What is the ERPF?
- effective renal plasma flow= the total amount of plasma going to the kidneys and thru the glomeruli
- difference btw ERPF and GFR
- GFR is only a fraction of total plasma flow, it represents only one glomerulus; ERPF represents the collective glomeruli
- What substance was used to determine ERPF?
- para-aminohippuric acid (PAH)
- What was ERPF determined to be?
- 585 mL/min
- How much of this goes out the efferent arteriole (not being filtered)?
- 585 - 125 = 460 mL/min
- %age of renal blood flow that goes to glomeruli?
- 90%
- what is the total renal plasma flow-TRPF (amt delivered to whole kidney)?
- 585/0.9 = 650 mL/min
- What is hematocrit (hct)
- the fraction of blood composed of RBCs, usually 45%
- approx amt of RBF-renal blood flow- total
- 1200 mL/min
- what %age of total blood volume is filtered each time around
- 21%
- What is the macula densa? What does it do
-
-the part of the tubule that passes thru the branches of the afferent/efferent arterioles
-detects change in sodium concentration and triggers vasoconstriction of afferent arteriole - What detects a BP decrease
- nearby granular cells with stretch receptors in teh afferent arteriole
- trace flow of filtrate thru the nephron
- glom caps release glomerular filtrate with enters the bowmans capsule then goes to PCT, the descending loop, the loop of Henle, the DCT, and then to the collecting duct
- where is H2O reabsorbed
- from the fluid in the descending interstitial tubule
- how?
- it maintains a constant fraction of the filtrate reabsorbed by the tubule leading to a constant rate of Na+ reabsorption and excretion
- action of Na+ and Cl- in ascending limb
- Cl- pumped out actively and Na+ pumped out passively
- What part of the nephron does ADH act on
- the collecting duct
- What does it do to the duct?
- causes holes to be inserted to increase H2O reabsorption
- how fast your kidney secretes a substance/drug is called
- clearance
- what organs are involved in clearance
- kidneys and liver
- why is it called virtual clearance
- b/c it doesn't measure how much substance is actually in the urine but rather how many individual mL of blood are cleared of the solute they're carrying.
- clearance equation
-
Cx = ([Ux] x V)/[Px]
clearance of x = concentration of x times volume of urine divided by plasma concentration of x - clearance
- the volume of plasma cleared of X
- why is creatinine used
- b/c its not reabsorbed and it's freely excreted
- where is creatinine normally found
- striated skeletal muscles
- easiest to measure: plasma creatine or urine creatinine
- plasma
- high conc of Cre plasma =
- poor renal function
- low conc of Cre plasma =
- person is sick
- does creatinine clearance measure GFR exactly
- no- overestimates GFR slightly b/c it's slightly secreted
- why is that important
- b/c it can miss early renal failure
- A decrease in GFR is often indicative of what
- ARF
- What does decreased GFR do physiologically
- dec.'d urine production (anuria or oliguria), creatinine clearance, and urea clearance
- dec'd creatinine clearance =
- inc'd plasma creatinine
- dec'd urea clearance =
- inc'd BUN
- azotemia
- inc'd plasma cre and inc'd BUN =
- azotemia is indicitave of ---
- ARF
- NL urine output =
- 750-2000 mL/day
- oliguria =
- = <500 mL/day
- anuria =
- = <100 mL/day
- polyuria =
- = >2500 mL/day
- What is the most important determinant of body fluid volume
- sodium
- how measured?
- Fraction Excretion of Na+
- Fractional Excretion of Na+ tells what
- quantifies the percentage of filtered sodium that is actually excreted in the urine.
- FE Na+ =
- = (UNa x Pcre)/(Pna x UCre) x 100
- FE Na+ when excess Na+ intake =
- up to 5%
- FE Na+ when too little Na+ intake =
- low as 0.1%
- sodium in the body fluid volume is a collective measure of...
- Na+ in extracellular space, including the plasma
- if little Na+ intake, filterted Na+ is ....
- conserved (reabsorbed).
- if too much Na+ intake....
- it's excreted
- Inc'd FE Na+ is usually a good indicator of ....
- the presence of a physiologic stimulus for the retention of sodium by the kidneys
- what are some physiolgical stimuli for Na+ retention?
- dehydration, x-treme blood loss, heart failure
- circulating fluid volume measures what?
- blood perfusion
- poor perfusion (an inc'd FEna) leads to
- dec'd GFR, dec'd urine output and azotemia (in'd BUN and Cre plasma)
- pre-renal failure or pre-renal azotemia
- the kidneys are not getting enough blood flow to do their job of filtering the plasma
- are the kidneys ill in pre-renal azotemia?
- no- the kidneys themselves are still OK, but the stuff being delivered to the kidneys, the circulation, is inadequate.
- what do kids do if they detect pre-renal azotemia?
- start conserving sodium in order to pump up the circulating fluid volume, so FE Na goes down
- FE Na in pre-renal azotemia =
- < 1%
- Intrinsic Renal Failure (Structural renal failure)
- kidneys themselves are sick, but blood flow is adequate
- post-renal failure (obstructive renal failure)
- both the kidneys themselves and the circulation to them are both OK, but there is an obstruction to urine output
- FE Na in renal azotemia
- > 1%
- if renal azotemia is intrinsic what happens to UNa and Uosm?
- Una in's and Uosm dec's
- What is ARF?
- abrupt decline in renal fx: dec’d GFR and therefore dec’d excretion of nitrogenous waste, dec’d urine output
- are most forms of ARF reversible
- yes
- What is uremia?
- azotemia w/ Sx
- what are the sx of uremia? 11
-
-N/V and anorexia
-pruritis
-yellow pigmentation
-weakness
-myalgia/twitching
-peripheral neuropathies (stocking, feet, and glove sensation loss; and loss of proprioception)
-dysrhythmias
-pericarditis
-anemia
-anion gap acidosis
-lethargy, confusion, seizures, coma - What causes pre-renal ARF
- hypotension or edematous states
- what would cause hypotension
- sepsis, volume depletion (blood loss, dehydration, hemorrhaging, untreated burns, diarrhea)
- what causes edematous states?
- CHF (loss of fluid volume into tissue), cirrhosis of the liver (hydrostatic pressure builds up, fluid leaves filling abdom cavity), nephrotic syndrome (xs protein in urine c/b leaky glomeruli; water leaves too and changes osmotic pressure)
- What is affected in intrinsic renal failure
- renal parenchyma
- The types of intrinsic (5):
- acute tubular necrosis, glomerulonephritis, interstitial nephritis, Infectious interstitial nephritis , and vasculitis (SLE)
- causes of acute tubular necrosis
- ischemia to kidney parenchyma, or nephrotoxic drugs
- what are nephrotoxic drugs?
- aminoglycosides (streptomycin and gentamicin) or radiocontrast drugs (no CT Scans!)
- What is the major Sx of glomerulonephritis?
- proteinuria
- most common cause of post-renal failure:
- uric acid stones
- what causes uric acid stones?
- hyperuricemia (i.e. from chemo)
- other causes of post-renal failure:
- nephrolithiasis or urolithiasis, tumors, BPH
- The 3 mechanisms kids use to regulate blood flow:
- myogenic, tubuloglomerulo-feedback, glomerulotubular balance
- does myogenic mech control GFR?
- partly
- how does myogenic work?
-
-Smooth muscles in vessels contract changing pressure and resistance.
-If P inc's arteriole muscle will contract and vessels constrict.
-Vessel constriction prevents inc'd P from causing inc'd blood flow - equation: P=
- Flow x Vascular resistance
- Which mech regulates GFR against momentary changes in BP?
- Tubuloglomerlu feedback
- what structure carries out tubuloglom feedback
- Juxtaglomerular Aparatus (JGA)
- components of the JGA=
- macula densa, granular cells, extraglomerular mesangial cells, and sympathetic nerves
- where is macula densa located
- btw. the efferent and afferent arteries
- what does macula densa do
- detects even a slight inc in GFR due to increase in flow to distal tubule and increase in NaCl concentration
- what happens when mac densa detect inc in flow rate?
- sends signal to granular cells wich cause afferent arteriole to constrict causing GFR to decrease
- what do extraglomerular mesangial cells do?
- secrete chemical junk and respond to inflammation
- what does the glomerulotubular balance mechanism do?
- keeps amount of filtered solute (NaCl) constant; prevents increase in Na+ loss while GFR is temporariy inc'd (due to inc'd BP)
- what are cause of acute changes in BP
- posture changes (sitting/laying), or brief exercise
- does kidney have parasympathetic innervation
- no, sympathetic only
- where do sympathetic fibers to the kidneys go?
- to the smooth muscle cells in all arteries and arterioles
- effect on arterioles?
- vasoconstriction
- branches of symp nerve fibers also innervate---
- granular cells
- activation of granular cells leads to what?
- gran cells secrete renin, leading to angio II which is a powerful vaso constrictor
- which two adrenergic receptors are involved in symp nerve stimulation
- alpha 1 and beta 1
- fx and location of alpa 1 receptors:
- located mostly on renal arterioles; : Sympathetic fibers innervating renal arteries release norepinephrine and cause vasoconstriction of the arteries/arterioles via alpha receptors
- what does this do to the renal blood flow (RBF) and GFR?
- decreases both of them
- where are beta 1 receptors located
- in granular cells of JGA
- beta 1 receptor fx:
- norepinephrine is relased from symp nerve branches and binds to beta-1 receptors. The agonism of the B-1 receptor causes renin release from the granular cells.
- what is end result of norep release
- increase in Na+ reaborption to keep fluid volume up
- 4 functions of Sympathetic NS activity in kids:
-
1. regulate blood flow to kids
2. regulate GFR
3. regulate renin secretion
4. regulate salt/H2O reabsorption - does plamsa NLy get filtered into tubular fluid?
- on each pass through the glomeruli, some of the plasma gets filtered into the tubular fluid
- active secretory/transport mechanism of tubular cells does what to drugs/toxins
- "sucks" them out of the peritubular capillaries & interstitium and secrete them into the tubular fluid (early urine)
- why are many toxins not readily filtered into the tubular fluid by the glomeruli
- b/c they bind to albumin
- what do lungs do in acid-base disturbances
- they increase or decrease ventilation (i.e blowing off or retaining CO2
- what do the kids do in acid base disturbances
- adjust the secretion and reabsorption of H+ and HCO3-ions
- what does aldosterone do
- increases Na+ reabsorption (Na conservation) and increases K and H secretion into tubular fluid
- What happens if theres too much aldosterone
- plasma Na increases, leading to water retention and an increase in the total circulatory fluid volume⬦and at the same time K+ and H+ are being secreted and dumped, so hypokalemia and increased plasma pH (alkalemia) both occur
- In dehydration, how high is the plasma osm?
- > 290mosm/L
- How does the hypothalamus monitor osmolality?
-
--the preoptic/periventricular nuclei of the hypothalamus fire action potentials down their axons to their ends in the posterior pituitary
--upon arrival, they stimulate the release of ADH from the axon terminals into the blood
--Then, ADH travels to the peritubular capillaries where it causes the development of new pores in the collecting ducts, through which excess water in the collecting duct fluid can be reabsorbed and retained by the body - what is diuresis
- denotes increased Na and water excretion by the kidneys
- T/F it takes several days without enough dietary calcium intake to signal the parathyroid to produce PTH
- F- less than a day
- During filtration, fluid and substances filtered into the proximal tubule are quickly reabsorbed by the proximal tubule cells and carried back into the circulation by the what?
- peritubular capillaries
- When the charge in the glomerular barrier disappears due to glomerulitis, the filtration barrier becomes excessively leaky to what?
- RBCs and plasma proteins.
- Why is PAH used to determine ERPF?
- because all of the PAH in the plasma (from the collective afferent arterioles) gets into the tubular fluid (and urine), whether by filtration or secretion
- about what percentage of the plasma flow thru the collective glomeruli is being filtered?
- approx 21%
- What happens to H2O in the descending limb of the loop of Henle
- it's passively reabsorbed
- What happens to Na in the ascending limb?
- its passively reabsorbed
- What does the passive reabsorption of both Na and H2O do?
- it removes water and traps Na (and urea) in the interstitium surrounding the bottom of the loop of Henle
- what is this cyclic mechanism called?
- a counter current multiplier system
- What does the counter current multiplier system do to osmolality
- It creates very high interstitial osmolality, 1200 mOsm, at the bottom of Henle’s loop (especially deep within the kidney..the medullary area), which is at about the same renal tissue depth as much of the collecting duct.
- When ADH is released and H2O is sucked out of the collecting duct, is the high osmolality diluted?
- no, because the peritubular capillaries take it away, and because the countercurrent multiplier mechanism works to maintain the high osmolality. Without maintenance of the high osmolality, and without ADH, we would all more easily come close to dangerous levels of dehydration.
- What are the units by which renal clearance is expressed?
- mL/min
- T/F Since creatinine is produced at a constant rate, plasma concentration of creatinine should also be constant if clearance of creatinine is also constant and in the correct range
- T
- What specifically, causes prerenal azotemia?
- burns, hemmorhage, dehydration, edema, CHF, renal stenosis, sepsis
- what is a common cause of acute tubular necrosis
- blood loss during trauma or surgery
- What are the 3 edematous states that cause prerenal ARF?
- CHF, liver cirrhosis, and nephrotic syndrome
- a specialized segment of the thick ascending limb of the nephron which passes
- macula densa
- Sum up the kidney's response to a decrease in BP
-
*Kidney puts out renin -> Angiotensin II production -> systemic vasoconstrictor increases BP.
*In addition to causing vasoconstriction, Angiotensin II also has the following effects:
**Angiotensin II -> causes release of ADH from posterior pituitary -> increased water reabsorption in the collecting duct -> increased circulating fluid volume ->increases BP
**Angiotensin II -> increases aldosterone from the adrenal cortex -> increased sodium reabsorption in the renal tubules, which itself causes more water to be reabsorbed from the tubular fluid - if you reclaim an extra 2% of total filtered Na per day, how much circulating fluid would that occupy?fluid
- 3.6L
- T/F the renin-angiotensin II aldosterone mechanism is a short term regulator of BP
- F- a long term regulator
- what are the four functions of sympathetic NS activity?
-
1. regulate blood flow to the kidneys
2. regulate GFR
3. regulate renin secretion
4. regulate salt and water reabsorption - what are the 2 mechanisms that regulate BP long term
- angiotensin II, aldosterone/ADH
- which of these induces vasoconstriction
- angiotenin II
- which of these regulates circulation of fluid volume
- Aldosterone/ADH
- What are the three primary detectors to control renin secretion
- high pressure baroreceptors in the carotid sinus and aortic arch, intrarenal baroreceptors, macula densa cells
- What happens when high pressure baroreceptors in the carotid sinus and aortic arch detect inc'd BP?
- causes an increase in sympathetic activity, which causes granule cells to release renin, leading to angio II production and thus global vasoconstriction which inc's BP and renal blood flow
- What else does Angio II cause?
- aldosterone secretion by the zona glomerulosa of the adrenal glands which causes inc'd renal sodium reabsorption, thus inc'ing circulating fluid volume and inc'ing BP
- intrarenal baroreceptors are also called what
- granular receptors
- how do granular cells detect pressure changes
- stretch receptors
- what do they do if low BP is detected?
- renin secretion, etc. (as before)
- what do macula densa cells do
- detect a decrease in tubular flow and NaCl content
- what happens when they detect changes?
- they decrease the release of chemical junk transmitters that NLy inhibit the release of renin from the granular cells resulting in an inc in renin, etc (as before)
- increased vasoconstriction
- angio II
- increased Na reabsorption
- aldosterone
- increased reabsorption of H2O into collecting duct
- ADH
- what percentage of all of the filtered Na does aldosterone control?
- 2%
- how many mEq can be reclaimed by aldosterone
- 504 mEq
- how do the kids play a role in CHF?
- a failing LVent causes a decrease in CO which dec's renal perfusion
- what do the kids do in response to decreased renal perfusion?
- secrete renin-angio II-vasoconstriction-inc total peripheral resistance (TPR)- inc BP
- An increase in TPR also causes what?
- increased ventricular work leading to increased cardiac sympathetic tone that's needed to help the failing LV able to handle pumping CO thru inc'd resistance. inc'd sympathetic tone also causes inc's renal sympathetic tone, causing renin secretion--viscious cycle
- Angio II further complicates CHF by releasing aldosterone. what does this do?
- inc's Na and Cl reabsorption in collecting ducts inc'ing circulating volume which leads to pulmonary edema, peripheral edema (ascites). this edema means a high vascular resistance packed tight w/ extra fluid leading to weight gain.
- Angio II further complicates CHF by releasing ADH. what does this do?
- inc's H2O reabsorption which inc's circulating volume (and thus BP)
- how do you treat CHF?
- diuretics and blood vessel dialators
- how does the nephron deal with glucose
- by co-transporting with Na or a.a.'s
- how much gluc is reabsorbed by the proximal tubule
- 100%
- what causes gluc to not be reabsorbed
- when the plasma load causes the filtered load to exceed the transport max (Tm) for glucose
- what is the Tm for glucose
- 375 mg glucose/min
- plasma glucose in a NL person=
- 1 mg/mL
- filtered load=
- volume of flow x concentration = 585 mL/min x 1 mg/mL
- plasma load=
- 585 mL of glucose/min
- filtered volume of glucose
- 125 mg/min of glucose get into tubular fluid
- T/F if the amt of filtered glucose per minute does not exceed the transport max, there will be zero glucose in the urine
- T
- how much glucose will go in the afferent arteriole and back out the efferent arteriole per minute
- 460 mg
- how much will get filtered (and also reabsorbed)
- 125mg/min
- what does extra glucose in the tubules do?
- leads to osmotic diuresis causing polyuria, polydipsia, and polyphagia
- T/F kidney regulates the plasma glucose concentrations
- F- insulin and pancreas do that
- T/F a.a.'s are too large to be filtered
- F- they are small enough and they get loosley bound to Na
- What proteins get into the tubular fluid and why in the case of multiple myeloma? What happens to the transport max?
- Bence-Jones proteins--b/c They are small enough that they are easily filtered. it causes Transport max for protein reabsorption to be exceeded so the excess over the max is released in the urine
- What is the result of xs sodium intake
- inc's extracellular fluid volume (ECFV) slightly b/c NaCl holds H2O
- what are the 4 major results of an inc in ECFV
-
1. decreased tubular reabsorption of Na (inc'd sodium excretion by the tubules)
2. pressure natruresis
3. decreased BP
4. increased GFR (and thus pressure natruresis) - What causes dec'd tubular reabsorption of Na?
- ECFV increase stretches pressure receptors in the R. atrium and pulmonary vessels wich signals the brain to decrease sympathetic activity which dec's renin which dec's angio II which causes dec's na reabsorp
- How does increased ECFV cause pressure natruresis
- it inc's BP so pressure natriuresis is due to slightly increased GFR despite regulatory mechanisms that try to maintain GFR stable. This helps excrete some of the excess NA.
- What does this slight increase in BP do?
- decreases renin/angioII/aldosterone/ADH which all dec BP
- How does the increase in BP lead to pressure natruresis?
- incd' BP signals barorecptors to inhibit sympathetic tone which dilates afferent arterioles and inc's the GFR causing pressure natruresis
- what happens to GFR if arterioles are dilated
- increases
- what happens to GFR if efferent arteriole is constricted
- increases: increases the filtration pressure in the glomerular capillaries so the GFR increases (think of a garden hose)
- what is an ACE inhibitor
- they cause dilation of the EFFERENT ARTERIOLE which decreases filtration pressure in the glomeruli
- How does glucose normally reenter the blood?
- Tubular cells pump glucose, co-transported with Na, back into the interstitium and glucose reenters the blood
- how is the rate of glucose clearance from the blood determined?
- Glucose Clearance = Ugluc * volume of urine / Pgluc
- T/F in a normal person, all of the glucose remaining in the plasma would be taken up by brain tissue and skeletal muscle with the aide of insulin
- T
- T/F It is normal for 250 mg/min of glucose to be in the urine
- F- shouldn't be there
- in treating CHF, what do diuretics do?
- they inc. excretion of Na, and therefore water leading to decreased BP & dec'd edema and less difficult for heart to pump
- What kind of CHF drugs dilate blood vessels?
- Calcium channel blockers, ACE inhibitors, and Angiotensin Receptors Blockers (ARBs)
- What do Ca channel blockers do?
- block the contraction of arteriolar smooth muscle which causes vasodilation--making it easier for heart to pump blood to kidneys and elsewhere
- What do ACE inhibitors and ARBs do?
- block production or function of Angiotensin II. – so also block the production of aldosterone and ADH
- when aldosterone causes retention of sodium, why is a proportional amount of water retained also by the kidneys?
- in order not to increase plasma osmolality beyond the normal 280-290 mOsm/Lt
- T/F When the kids secrete renin and create the whole Angio II- aldosterone-ADH cascade, the rest of the body is not affected
- F- they do it to serve themselves but it affects are systemic
- T/F kidneys eliminate volatile acid
- F
- T/F lungs eliminate volatile acid
- T
- T/F H2CO3 is a volatile acid
- T
- T/F H3SO4 and H2PO4 are nonvolatile acids
- T
- What happens when the lungs get rid of CO2
- it forces the recombnination of H+ and HCO3-, forming H2CO3 again.
- H2O + CO2 yields what
- H2CO3 --> H+ + HCO3
- What is the net result of nonvolatile acids in daily metabolism?
- 1mEq H+/kg of body weight/day (50-100mEq/day)
- Where does SO4 come from?
- amino acid side chains- metabolism from our daily diet produces H2SO4
- What would happen if the kidneys could not eliminate this nonvolatile acid?
- [H+] would increase 60,000 times to .0024M (a pH of 1-2)
- what is normal tissue pH and H+ concentratiom?
- 7.4 or .00000004M
- What do the kids do if plasma/body pH decreases?
- inc's H+ secretion/excretion, inc reabsorption of bicarbonate, and inc creation of new bicarbonate
- What do the Na/H antiporters do?
- secrete H+ into tubular fluid and reabsorb Na+
- T/F this is a uni-directional exchange
- F- bidirectional
- Where are the Na/H antiporters located?
- proximal tubule
- where are the intercalated cells located
- in the collecting duct
- what are intercalated cells
- a type of tubular epithelial cell
- What lies on either side of the intercalated cells?
- interstitium and tubular lumen
- What type of pump is located in the intercalated cells?
- proton pump
- What does the proton pump do?
- pumps H+ ions up their gradient (from interstitium to tubular fluid)
- How high can the urinary concentration of H+ be before the pump fails?
- 1000 times normal (3 pH units)
- What else is necessary for the pump to work?
- a buffer in the tubular fluid
- What are examples of buffers in this case?
- NH3 and HPO4-