Physio Exam 3 Renal 4

Front 1

Thick ascending limb is known as

Back 1

Diluting segment because H2O is impermeable but NaCl is reabsorbed

Front 2

Na+ reabsorption in the thick ascending limb is load dependent meaning

Back 2

Amount of Na pumped by NKCC2 is load dependent. The more Na the more reabsorbed.

Front 3

The NKCC2 pump utilizes

Back 3

Na gradient

Front 4

What maintains the [K] in the thick dascending tubule?

Back 4

H channels on apical membrane

Front 5

In the thick ascending tubule Na is also absorbed via

Back 5

H secretion

Front 6

As compared to the proximal tubule, thick ascending limb's reabsorption of HC03 is

Back 6

smaller

Front 7

Cation paracellular diffusion (Na, K, Ca, Mg) in the thick ascending tubule due to

Back 7

the positive electrical gradient established

Front 8

Loop diuretics inhibit NKCC2 as a consequence

Back 8

consequence more NaCl loads delivered to distal part of nephron so as a consequence impair Na and water reabsorption of collecting tubules=diauresis

Front 9

Barttter's Syndrome affects the thick ascending limb, what this occurs due to mutation in NKCC2

Back 9

Mutation in the NKCC2, ROMK, or ClC-Kb channels cause an inhibition of NaCl
and K reabsorbtion in the TAL via the NKCC2 pump. This results in an increase
in Na+ delivered to the distal tubule and conducting duct, resulting in salt depletion
and polyuria, triggering the renin-angiotensin-aldosterone pathway. Hyperaldosteronism
causes hypokalemic metabolic alkalosis.

Front 10

Bartters Syndrome can also be caused by a mutation in K channel leading to

Back 10

same consequences as the mutation of NKCC2, in this case, mutation prevents back lead of K so NKCC2 function is compromised

Front 11

Another Bartter's Syndrome mutation occurs in Cl channel mutation, leading to

Back 11

elevation in intracellular Cl, NKCC2 is inhibited because it relies in the Cl gradient

Front 12

Transport characteristic of the early distal tubule

Back 12

Cortical diluting segment (Early distal tubule is impermeable to H20. This segment is the diluting segment because tubule is impermeable to water yet, NaCl is reabsorbed.)
Electroneutral Na+ Reabsorption

Front 13

Early Distal Tubule is the site of action of

Back 13

thiazide diuretica

Front 14

Electroneutral Na reabsorption in the early distal tubule is achieved by

Back 14

Na/Cl symporter, Na and Cl into cell depending on Na gradient established by Na/K basolateral pump

Front 15

Transport by the late distal tubule and collecting tubule

Back 15

The collecting tubule sees the appearance of principal cells and intercalated cells

Front 16

Principal cells job

Back 16

Na+ Reabsorption (ENaCs)
K+ Secretion
Variable H20 Reabsorption (AQPs)

Front 17

K secretion from principal cells is induced by

Back 17

Aldosterone

Front 18

Variable H2O reabsorption is induced by

Back 18

ADH-.AQP

Front 19

Intercalated cells job

Back 19

Secrete either H+ or HCO3-
Acid/Base balance
Reabsorb and regulate K+

Front 20

Hyperkalemia (elevated K) effect on action potential

Back 20

elevation
of Resting Membrane Potential and inactivation of fast Na+ channels,

Front 21

Hypokalemia effect on Resting membrane potential

Back 21

moves the RMP further
from threshold. In the heart, alterations in
K+ can also cause abnormalities in
repolarization.

Front 22

Cardiac arrhythmias are produced with
both

Back 22

hypo- and hyperkalemia

Front 23

in terms of K balance The kidneys have the ability to

Back 23

remove a lot of K

Front 24

Immediate regulation of K balance

Back 24

: Alter the internal K+ balance by altering the distribution of K+ between ICF and ECF. Minute to minute

Front 25

Long term regulation of K balance

Back 25

Alter the external K+ balance by altering the urinary excretion of K+. Effective
after about 6 hours

Front 26

Homeostatic regulatory mechanisms of internal K balance

Back 26

Insulin
Aldosterone
Epinephrine

Front 27

Insulin

Back 27

Stimulates K+ uptake into muscle,
liver, bone via stimulation of
Na/K ATPase, NKCC1, NaCl
symporters. In contrast, diabetes
mellitus produces hyperkalemia

Front 28

Aldosterone

Back 28

Similar to insulin, induces K+ uptake
but takes longer (60 minutes)

Front 29

Epinephrine:

Back 29

Epinephrine release stimulated by
elevated plasma K+ as well as
β2 agonists induce cell uptake
similar to insulin. α agonists can
produce the opposite, resulting
in hyperkalemia.

Front 30

Abnormal Plasma K can be caused by

Back 30

Acid-base
Osmolarity
Exercise
Cell Lysis

Front 31

whats used to buffer acid-base shifts?

Back 31

: The cellular H+/K+

Front 32

Metabolic
Acidosis can produce

Back 32

hyperkalemia

Front 33

Metabolic Alkalemia can produce

Back 33

hypokalemia

Front 34

acid base shifts leading to abnormal K production also involve direct inhbition of

Back 34

Na/K Atapse and NKCC1

Front 35

Hyperosmolarity causes

Back 35

Hyperkalemia. As water leaves
cells, ICF becomes hyperosmolar
and K+ diffusion gradient increases
as intracellular [K+] increases

Front 36

Minor hyperkalemia can be caused by

Back 36

increased muscle activity, but this minor hyperkalemia is important for local control of blood flow

Front 37

. Rhadomyolysis and
tumor lysis syndrome (cell lysis) can cause

Back 37

: High cellular K+ can produce hyper-
kalemia.

Front 38

The regulatory event of external K balance is

Back 38

regulated K+
secretion by
principal cells
in the late
distal tubule
and collecting
duct. Only place where K is regulated.

Front 39

Regulated secretion of K by principal cells depends on

Back 39

1)Concentration gradient across the principal cell established
by Na/K ATPase (If Na/K activity goes up, more Na out, K in, concentration gradient and K would be secreted through K channel at greater levels)
2)The electrical gradient
generated by the reabsorbtion of Na thru E-Na channels (If Na reabso stimulated, intracel more positive, K out of cell into lumen of nephron
)
3)The K+ permeability of the
apical membrane

Front 40

Hyperkalemia effect on principal cells

Back 40

stimulates Na/K ATPase
increases apical K+ permeability
increases tubular flow rate
increases aldosterone secretion

Front 41

Hypokalemia effect on principal cells

Back 41

inhibits Na/K ATPase
reduces apical K+ permeability
reduces tubular flow rate
reduces aldosterone secretion
increase reabsorbtion via the H+/K+
exchanger in intercalated cells

Front 42

Chronic Hyperkalemia effect on principal cells

Back 42

increase Na/K ATPase
increase ENaC
increase Serum Gluccocorticoid-
stimulated Kinase
increase Channel Activating
protease
increase K+ channel permeability
increases mitochondrial activity
to support energy expenditure

Front 43

Aldosterone stimulated by

Back 43

Ang II or by hyperkalemia

Front 44

ECF volume or diuresis effect on tubular flow rate

Back 44

Increases Na+ load delivered
to distal tubules and collecting
duct and elevates principal cell
[Na+], enhancing electrical gradient
and stimulating Na+/K+ ATPase
2)Bending primary cilium of
principal cell activates Ca++
entry via PKD1/PKD2 calcium
channel, which activates K+
channels (Maxi-K, ROMK)

Front 45

Long standing chronic
Metabolic Acidosis such
as seen with diabetic
ketoacidosis can result in

Back 45

increased excretion
of K+. Plasma levels in
these patients can be
elevated because of a shift
in cellular K+ subsequent
to acidosis; however total
body K+ is reduced as
excretion is stimulated.

Front 46

Long standing chronic metabolic acidosis patients can be treated with insulin but this may lead to

Back 46

serious hypokalemia
and potential cardiac
arrhythmias, so plasma
K+ must be monitored
during treatment

Front 47

Short term metabolic acidosis effects

Back 47

; INHIBITION of Na/K Atpase and decrease in K permeability, secretion of K in principal cells decreased hence, so K in blood up, causing slight hyperkalemia

Front 48

Long term, acid load for longer time, shift of acid into cell which exchanges

Back 48

with K and pump K out of cell, K/h exchange increased, as a result, aldosterone is released. In the proximal tubule due to inhibition of Na/K Atpase, decrease in NaCl and H2O reabsorption hence tubule flow rate increases and extracellular fluid volume would decrease, more water excreted..aldosterone goes up at collecting tubule and distal tubule and K secretion would increase, so we would be depleting intracellular stores developing into hypokalemia.