Renal III

Question 1

CKD cycle

Answer 1

damage glomerulus
less NaCl in macula densa
TGFeedback increases renin
ang II causes EA constr.
can cause more damage

Question 2

what diseases can magnify CKD?

Answer 2

hypertension

diabetes

Question 3

what type of acid base imbalance is caused by CKD?

Answer 3

metabolic acidosis

Question 4

waste products are dependent on what to be filtered?

Answer 4

GFR

as GFR decreases more waste products will build up in the plasma

Question 5

phosphate and H+ are maintained at normal filtration UNTIL?

Answer 5

GFR falls under 30% of normal

bc the kidney has high baseline excretion rates and hormonal influence

Question 6

electrolytes are maintained UNTIL?

Answer 6

renal failure

dialysis is used to maintain function

Question 7

what does metabolism of macronutrients produce?

Answer 7

significant volatile acid load (CO2) ~15,000 mEq/d
small nonvolatile acid load
~70mEq H+/d

Question 8

what are the 3 systems used to buffer the acid produced daily?

Answer 8

rapid ECF buffer by HCO3- and phosphate
rapid pulm exhalation
slow renal excretion of H+

Question 9

what does the kidney use to buffer H+?

Answer 9

NH3 and Phosphate

Question 10

normal H+ value

Answer 10

40mEq/L

Question 11

what detects changes in pH?

Answer 11

peripheral chemoreceptors in carotid and aortic bodies

Question 12

what alters respiratory control centers in medulla?

Answer 12

PaO2 and PaCO2

Question 13

as you increase alveolar ventilation by 2 how much does that increase pH

Answer 13

.2 increase in pH

Question 14

why are there two systems working here?

Answer 14

compensation

Question 15

acute disturbances

Answer 15

less time and less compensation

Question 16

chronic disturbance

Answer 16

more time and more compensation

Question 17

what does compensation do?

Answer 17

helps normalize pH but does NOT correct the original disturbance

Question 18

3 major acid-base functions of the kidney

Answer 18

excretion of fixed metabolic acids
regulation of plasma HCO3-
protect from bad buffering

Question 19

what is bad buffering?

Answer 19

proteins can buffer but it alters their function

Question 20

what % of filtered load of bicarb is excreted in the urine?

Answer 20

0%

Question 21

how much bicarb is filtered and reabsorbed?

Answer 21

4320mEq

Question 22

what promotes H+ secretion/HCO3- reabsorption?

Answer 22

acidosis
hypokalemia
aldosterone or ang II
decrease in ECF volume (more Na/H activity)

Question 23

what is the pH of normal urine

Answer 23

6 or less

Question 24

what does Ang II do to the Na/H transporter

Answer 24

increased activity

Question 25

what does increased acid load do to HCO3 transporters?

Answer 25

increases the amount of transporters | unknown mechanism

Question 26

where is the majority of H+ secretion happen

Answer 26

PT

Question 27

what parts or cells are used for H+/HCO3- management during normal to acidosis?

Answer 27

PT, TAL, DT, CD | type A cells

Question 28

what type of cells or parts are used for H+/HCO3- management during alkalosis?

Answer 28

DT, CCD | type B cells

Question 29

when there is more K in the lumen what does the type A cell do

Answer 29

takes up more K and secretes more H+ and can put you at risk for alkalosis in the blood

Question 30

what do type B cells do

Answer 30

bicarb secreted via HCO3-/Cl- exchanger | renal H+ reabsorb

Question 31

can type A turn into type B cell when in sustained alkalosis?

Answer 31

yes evidence to support this

Question 32

A low and normal dose of Diamox (acetazolamide) blocks Carbonic Anhydrase (mostly in the PT) and is commonly Rx’d to treat glaucoma. Will the urine be acidic or alkaline?

Answer 32

alkaline

Question 33

why can alkalosis cause hypokalemia

Answer 33

because the HCO3- in the lumen causes the K+ channels to be open & establishes an electrochemical gradient more K+ is secreted or excreted

Question 34

what does acute acidosis decrease

Answer 34

all ATPase transporter activity | the open probability of the K+ channels (hyperkalemia?)

Question 35

what does chronic acidosis increase?

Answer 35

-sk.m. H+/K+ exchanger (increase [plasma K+] -reduce Na/KATPase acticity (lowers ECFV) -both of above increase aldosterone -higher flow rates and aldosterone promote K+ secretion HYPOkalemia!!

Question 36

where has most of the H+ in the tubular lumen come from

Answer 36

built up from tubular secretion

Question 37

can bicarb serve as the renal base?

Answer 37

no bc we need to reabsorb it

Question 38

what is the maximal free H+ of the urine?

Answer 38

0.03mmol/L

Question 39

what are the primary filtered renal buffers?

Answer 39

phosphate and ammonia

Question 40

what are large acid loads excreted mainly in the form of?

Answer 40

ammonium

Question 41

which renal buffer can adapt to meet demand?

Answer 41

ammonia phosphate stays around the same level (increases slightly)

Question 42

where is glutamine synthesized

Answer 42

the liver from NH4 and bicarbonate

Question 43

what happens to glutamine when it reaches the proximal tubule?

Answer 43

converted into 2 new bicarbs and 2 NH4

Question 44

where is ammonium reabsorbed?

Answer 44

the TAL by NKCC

Question 45

what happens to ammonium in the CCD?

Answer 45

it is secreted from the interstitial fluid via NaK pump and HATPase