Physio Exam 3 Renal 8

Front 1

Main Cation in the ECF

Back 1

is Na, main anion in ECF is Cl followed by HCO3 and then albumin.

Front 2

AG equation

Back 2

[Na-(Cl+HCO3)]

Front 3

Normal anion gap

Back 3

is 8-12..this range is because some labs measure Cl differently. Electroneutrality must be maintained. If HCO3 level drops then either Cl goes up or anion gap has to go up…this if Na stays constant.

Front 4

Anion gaps is the unmeasured anions in the plasma and the unmeasured anions are

Back 4

albumin, ketoacids, lactic acid, phosphate, sulfate, and organic acids

Front 5

Henderson Hasselback Equation

Back 5

pH=6.1+log HCO3/H2CO3

Front 6

H2CO3 not measured directly but via

Back 6

PCO2

Front 7

HCO3 mostly regulated by

Back 7

Kidnet and PCO2 by lungs
Metabolic HCO3
Respiratory 0.03XpCO2

Front 8

Reabsorbs 70% of the filtered HCO3

Back 8

Proximal Tubule

Front 9

Methods of HCO3 transport in proximal tubule are

Back 9

Na-H exchanger
Basolateral Na-HCO3 cotransporter

Front 10

Reab of HCO3 in the proximal tubule is influenced by how much

Back 10

Na absorption there is, the more Na reab the more HCO3, also influenced by availability of CO2, if CO2 high lots of acid secreted

Front 11

see PROXIMAL TUBULE HCO3 Transport

Back 11

H gets secreted and a OH is generated, Na gets absorbed, inside the cell theres gas CO2 which reacts with OH by the activity of Carbonic Anhydrase generating HCO3 is formed which is transported through basolateral membrane via Na/HCO3

Front 12

HCO3 reab of GFR greater than 28 (Tubular Max) leads to

Back 12

HCO3 starts being excreted in urine. This dependents on Na. During volume contraction so Na is needed, then it will be reab leading to more HCO3 reab as well. Na is retained to retained water (volume contraction=volume is low). In cases of volume expansion, Na reab will go down, and hence HCO3 will also go down.

Front 13

Factors Influencing ProximalHCO3 Reabsorption
Volume Contraction
Volume Expansion
pCO2
pCO2
Angiotensin 2
Carbonic Anhydrase Inhibition
Hypokalemia
Hyperkalemia

Back 13

Increase
decrease
increase
decrease
ubcrease
decrease
increase
decrease

Front 14

When plasma K is lost, how do we get back to normal levels

Back 14

From muscles, and to move K, H exchange is needed. Hypokalemia is associated with accumulation of H intracellulary hence leading to low pH and intracellular acidosis..so HCO3 reab will be enhanced

Front 15

Hyperkalemia leads to K absorption, because high K leads to depolarized membrane pitential in

Back 15

the heart and death..as consequence, H is pumped out and leading to less HCO3 reab

Front 16

Acid produced in the form of

Back 16

phosphate and sulfate.These acids consume HCO3

Front 17

Distal nephron regenerates

Back 17

HCO3

Front 18

Acid secretion in the HCO3 mediated by

Back 18

H+ATPase

Front 19

Acid is secreted in urine as

Back 19

ammonium and titrable acid

Front 20

Vegetable diets don’t have a lot of acid as compared to meat protein..vegetarians produce what type of diet?

Back 20

alkaline diet

Front 21

In cases when acid is not excreted, it is retained and bone disease

Back 21

develops like rickets

Front 22

slide 16

Back 22

Need to secrete acid in urine;
Proton secreted and buffer is generated. Secretin proton without a buffer leads to inhibition of the H ATPase pump. NH3 is the buffer. It binds the secreted H+ and NH4 is made..and this is mainly how amonia is secreted in the urine.
Since a H+ was secreted, and OH was generated inside the cell which reacts with CO2 and Carbonic Anhydrase and HCO3 is generated which is pumped through basolateral membrane via a HCO3/Cl exchanger. Cl goes on to be secreted into the lumen, and once there it forms NH4Cl and is excreted into urine. Cl is excreted in 3 forms, NaCl, KCl and acid NH4Cl.
When theres kidney failure system is destroyed..no excretion of acid so patients have low HCO3 so dialysis machine compensates by adding HCO3

Front 23

Distal nephron has two main cells

Back 23

Principal cells and Intercalated cells

Front 24

Principal cells main job

Back 24

Na reab

Front 25

Intercalated cells main job

Back 25

H reabs

Front 26

Principal cells has a Na channel and it gets pumped via across basolateral via Na/K..K pumped into cell gets later secreted into urine. Not shown in this pic Cl is less permeable than Na, then theres a separation of charge, so Cl lags behind and Na goes across therefore in the lumen of distal nephron gets negative which favors

Back 26

K secretion..this mediated by aldosterone. This same negativity favors H secretion from intercalated cells.

Front 27

Principal cells have receptors for.....on its basolateral membrane

Back 27

Aldosterone

Front 28

Too much aldosterone on principal cells

Back 28

Na absorption goes up, and volume becomes expanded, blood pressure goes up, K secretion is gonna increase so blood K goes down developing hypokalemia too much H secreted and HCO3 added more to blood so more HCO3 in blood. This happens in primary hyperaldosteronism also in heart failure..a diuretic can be given to excrete Na

Front 29

No aldosterone effect on principal cell

Back 29

: Na reab goes down, blood pressure goes down, serum K goes up, urine K goes down, H is not secreted no HCO3 added to cell..acidosis will be developed

Front 30

Effects of aldosterone on distal nephron

Back 30

 Na reabsorption both by increasing Na channels and Na K-ATPase activity.
 The transepithelial voltage (lumen is more negative).
 K secretion.
 H+ secretion.
 NH3 production
All increase

Front 31

Clinical Implicaions of Increased Na reab in the collecting duct by aldosterone

Back 31

Na retention
Volume expansion
High blood pressure
Increased K secretion
Hypokalemia

Front 32

Distal nephron H+ secretion and components

Back 32

Intercalated cells or  cells.
H+ ATPase.
Role of H+ K-ATPase: unclear.
Steep H+ gradient.
Blood pH 7.4 – urine pH 4.4 = 1000 H+ gradient.
Low permeability of the lumen to H+.
Carbonic anhydrase II in the cell.
Cl-HCO3 exchanger in the basolateral membrane

Front 33

Urine test of distal acidification

Back 33

Good to detect bicarbonate in the urine
high urine pH: high HCO3 or infection with urease producing bacteria
Poor for ammonia excretion

Front 34

Acute Acidosis is

Back 34

Urine pH decreases to < 5.5

Front 35

CHRONIC ACIDOSIS

Back 35

H3 production increases
NH3 Buffers H+  NH4+
Low urine pH does not provide information about how much NH4+ is present in the urine

Front 36

URINE pCO2

Back 36

Reliable indicator of distal H+ secretion
H+ + HCO3 -> H2 CO3 -> CO2(up) + H2O

Front 37

URINE AMMONIA

Back 37

. Main urinary buffer.
2. Reliable indicator of acid excretion.
3. Not valid in presence of infection with
urease producing organisms.
4. Assay for urine ammonia usually not
available in clinical laboratory

Front 38

MAJOR CLINICAL MANIFESTATIONS OF DISTAL RTA

Back 38

. Hyperchloremic acidosis
2. Hyperexcretion of cations
a. Calcium
b. Potassium
c. Sodium
3. Nephrocalcinosis
4. Nephrolithiasis
5. Growth retardation
6. Osteomalacia
7. Renal insufficiency

Front 39

In regards to 1

Back 39

Amonia not pumped in urine (how H goes out in urine). Na-HCO3 being excreted, NaCl retained, so high Cl is developed and low bicarbonate

Front 40

In regard to 2

Back 40

Dumping K in the urine because acid cant be pumped out, acid gets buffered in bone so Ca2+ leaks out from the bone , kidney stone forms