Renal 15 Loh

Front 1

what cells are the target of ADH and ALDO, what do these do?

Back 1

late DCT principal cells

**ADH: water reabs
**ALDO: Na reabs

Front 2

what do the principal cells of the late DCT do?

Back 2

reabs Na
Secrete K

respond to ALDO (Na reabs)

Front 3

what do the a intercalated cells do?

Back 3

secrete H
Reabs K

Front 4

reabs of Na nad secretion of K in the late DCT depends on what

Back 4

Na/K ATPase and apical channels (aldo increases apical na and Na/K)

Front 5

the principal cells in the __ DCT abs ___ and secrete ___

this is regulated by ___

Back 5

late
Na
K

**aldo increases apical na and Na/K

Front 6

principals cells are important for
intercalated cells are important for

both are located

Back 6

Principal: na reabs
A intercalated: acid base balance (H secretion)

llate DCT

Front 7

aquaporins are added to what side of the membrane in what area of the nephron, what hormone

Back 7

apical
CD
ADH

Front 8

ADH works at the ______
ALDO works on _____

Back 8

CD
principal cells of late DCT

Front 9

what happens when ADH binds to its receptor in the basolateral membrane of teh Cd cells

Back 9

insertion of aquaporins on the apical membrane and water is allowed to be removed from the tubular lumen and enter the BV

Front 10

where is the most NaCl reabs? what isthe osm here

Back 10

PCT

**tubular fluid is isosmotic

Front 11

in the descending limb what happens? what is the osm if the tubular fluid

Back 11

H2O is reabs

*hyperosmotic

Front 12

what happens in teh ascending limb, what is the OSM of the fluid

Back 12

NaCl is reabs

**hyposomotic

Front 13

what happens int eh early DCT, OSM

Back 13

NaCl reabs, No H20 reabs

**hyposmotic

Front 14

what happens in the late DCT and CD? OSM

Back 14

Na reabs regulated by ALDO

H2O levels regulated by ADH

**can be hypo or hyperosm

Front 15

in the PCT NaCL is reabs but the fluid is isoosmotic. In the descending limb H2O is reabs and the fluid is Hyperosmotic. In the Ascending limb NaCl is reabs nad the fluid is hyposmotic. Same thing in early DCT, NaCl reabs, water is imperm and the fluid is hypoosmotic. In the late DCT Na and H2O reabs are controlled by ALDO and ADH respectively and the relative amts can create a hyper or hypoosmotic fluid

Back 15

sfdkj

Front 16

waht are the 3 wyas we protect against acid base disturbances

Back 16

1 buffer: HCO3, Hg, Pi. FAST
2 renal compensation: vary amt of HCO3, SLOW
3. respiratory compensation: alter CO2, often incomplete FAST

Front 17

of buffers lungs and kidneys what works the fastest, what can work the longest

Back 17

buffers and breathing are both really fast, buffers prbly work longer than breathing but KIDNEY works longest of all and can handle prolonged issues (NH4 for chronic acid overload)

Front 18

pH = 7.52
HCO3-= 22
PCO2= 28

wahts the deal

Back 18

1. pH Alkalosis

2. CO2 should decrease or HCO3 should increase.
CO2 is low--> RESPIRATORY, alkalosis

3. uncompensated bc pH is NOT within range and HCO3 didnt respond
**CO2 decreased by 10 so we expect HCO3 to decrease by 2

**caused by hyperventilating, kidney doesnt have enough time to work

Front 19

whats the deal

pH = 7.43
HCO3-= 18
PCO2= 28

Back 19

1. pH Alkalotic

2. CO2 decrease (40) 28, RESPIRATORY
HCO3 increase (22-26)
3. HCO3 should decrease by 2, but it decreased WAY lots so complete compensatiion

Completly compensated respiratory alkalosis, we hyperventalated but gave it some time and the kidney fixed the problem

Front 20

whats the deal

pH = 7.16
HCO3-= 14
PCO2= 41

Back 20

1. acidotic
2. metabolic
3. uncompensated

Front 21

acidosis is caised by waht canges in CO2/HCO3

Back 21

CO2 increase
HCO3 decrease

**respiratory if CO2, HCO3 is metabolic

Front 22

when we have compensation in what way do CO2 and HCO3 change? what if there is change in the undesired direction

Back 22

same direction

If CO2 increases and causes acidosis, HCO3 will also increase to try to compensate, if HCO3 also DECREASES we have a mixed acidosis

Front 23

name 3 things that cause metabolic alkadosis

Back 23

**increasing HCO3

1. ingestion of alkaline things (antacid)

2. lots of ALDO (conns syndrome). aldo stimulates H secretion via H+ ATPase uniport in the DCT

3. Volume Contraction: vomit, NG suction, loop/thiazide diuretics

Front 24

aldo does what to acid base balance

Back 24

it stim the H ATPase antiport in the DCT, lots of acid is secreted so we get alkalotic

**metabolic alkalosis due to increased acid secretion (this in turn increases HCO3 production)

Front 25

what causes increased H secretion in the DCT which leads to metabolic alkalosis? what is the transported that is manipulated

Back 25

ALDO acts on teh H uniport to get H secreted and thus make more HCO3

Front 26

what does volume contraction lead to, what are some examples

Back 26

metabolic alkalosis that is maintained!

1. Vomit: loose HCL, K, fluid
2. NG suctin, same as vomit
3. Thiazides (DCT) or loop diuretics: loose fluid and K

Front 27

what maintains metabolic alkalosis

Back 27

ECF contraction maintains alkalosis even after vomiting is done

Front 28

when fluid is lost what hormone is secreted? what does this lead to?

Back 28

renin

**ANG II -->stimulates Na/H antiporter and thus HCO reabsorption

**this is MAINTAINED alkalosis, we have decreased fluid so the body releases renin to hang on to it. this causes H to be secreted and HCO3 to be made in excess

Front 29

so we know ALDO can cause H secretion and HCO3 production due to stim at DCT via H uniport.

Under what condistions is there a similiar story but a different transported

Back 29

volume depletion, leades to renin release, leads to ang II release, causes the Na/H antiport to be active in PCT

**increase H secretion
**increse HCO3 abs

**even once the vomit and initial loss of HCL is done we have maintained alkadosis due to ANGT II stim H sectetion

Front 30

what does ANg II do to acid base balance, once specific set of conditins

Back 30

VOLUME DEPLETE

*decrease volume releases renin ---> ang 2 --> Na/H antiport active --> H secretion + HCO3 production --> metabolic alkadosis

**so in the case of vomit we are already alkalotic bc we lost HCL but we do a double whammy bc now we increase H secretin and HCO3 reabs via ANgT 2 Na/H antiport in PCT

Front 31

aldosterone stimulates secretion of ______ via ________ transported from _______ cells and ______ from ______ cells

Back 31

H
H uniport
a intercalated

K
Principal cells

Front 32

seeing what 2 things means that there will be maintained metabolic alkalosis

Back 32

1. hypokalemia ( ALDO stimulates K secretion in principal cells of DCT)

2. high ALDO

Front 33

what hapens to K in metabolis alkalosis

Back 33

increased secretion due to ALDO at DCT principal cells

**hypokalemia

**hypokalemia is one of the markers of prolonged alkalosis

Front 34

what does it mean that the nature of the kidney will maintain alkalosis when we are volume depleted

Back 34

the depleted volume stim renin ANG II ALDO

ANG II: PCT Na/H
ALDO: DCT H uniport

**H is secreted and HCO3 is made

Front 35

Metabolic alkalosis and ______ often linked, especially during _______

Back 35

hypokalemia
volume contraction.

Front 36

how does hypokalemia stim H secretion

Back 36

so we get hypokalemic when we are volume dpleted (metabolic alkalosis)

**low K stim K/H antiport in principal cells. Secreted H and Keep K

Front 37

we know having low K as is seen in alkalosis can stim H secretion in an attempt to save K, can hypokalemia do anything else

Back 37

stim Nh4 secretin, also induces more alkalosis

Front 38

in metabolic alkalosis is hypokalemia the only electrolyte imbalance we see

Back 38

nope,

also hypochloremia

Hypochloremia also stim H secretion

Front 39

damn this kidney! waht does hypochloremia stim

Back 39

H secretion! go figure the sx of metabolic alkalosis (low Cl) will further the alkalosis.

Front 40

what does chloride do in alkalosis with volume contraction

Back 40

1. decreased

1. ANG II and ALDO are high to recover water

3. this means H is being secreted and Na is being reabs

4. BUT... we dont ahve Cl to cotransport with Na

5. this makes the lumen of DcT (-) (Na+ is being lost, so - accumulates)

6. This - lumen drives H and K secretion

Front 41

how can you treat some forms of metabolic alkalosis

Back 41

with saline

gets volume back in order (initial problem)
gets electrolytes (k, Cl back in order)

Front 42

how does chloride saline help volume depleted metabolic alkalosis

Back 42

1. Fix Volume. Renin ANG ALSO turns off and we have less H sectetion, adn HCO3 reabs

2. Cl can now transport with Na, so the lumen of the nephron is less (-) and so wont attract H and K for secretin

3. thses all cause HCO3 excretion

Front 43

does saline help all cases of metabolic acidosis due to volume contraction

Back 43

nope, not conns. here we have an also secreting tumor. so the extra fluid wont stop the renin system

Front 44

can all metabolic alkalosis be treated with saline

Back 44

nope, not ALDO secreting tumors

Due to Na reabs that then favors H secretion and HCO3 production

Front 45

what is the formular for anion gap, is tehre usually a physiologically normal gap, why or why not

Back 45

Na - (Cl+HCO3)

notmally an 8-16mM gap, not all anions are measured!! there are less anions

Front 46

if someone has Na Cl nad HCO3 such that there is a 14 nM difference is this a problem

Back 46

not really, there is a normal anion gap **LESS anions than cations

Front 47

what does an anion gap mean

Back 47

less anions than cations

** Na - (Cl+ HCO3)

**several anions are not tested in blood samples

Front 48

is there an anion gap if you are experienceing acid base disequilibrium, in chich way

Back 48

Acidois, less HCO3 so a larger anion gap

**even LESS anions than normal

Front 49

so we know metabolic acidosis can be due to a decrease in HCO3 or an increase in acid what are soem specific wats this can happen. what can this be associated with

Back 49

1. acid ingestion
2, HCO3 lost from body in diarrhea
3. lactic acid builds up (exercise or hypoperfision)
4. decreased HCO3 recovery
5. Decreased NH4 excretion

**associated with a larger anion gap, missing HCO3

Front 50

what is renal tubular acidosis

Back 50

when you have metabolic acidosis bc you have decreased H secretion

Front 51

what are the 3 types of renal tubular acidosis, what is the underlying cause in each case

Back 51

decreased H secretion from the tubule
Type I: distal, H ATPase uniport isnt working

Type II: PCT, Na/H exchanger isnt working

Type 4: decreased NH4 secretion (main type for handling chronic loads). often due to hyperkalemia secondary to aldosterone deficiency; inhibits enzymes that degrade glutamine

Front 52

in type I RTA whats the problem

Back 52

excess acid in blood bc H isnt being taken up in the DCT by H uniport

Front 53

what is the deal in type II RTA

Back 53

increased acid bc the PCT cant secreted H, via Na/H antiport

Front 54

what is it called when the Na/H isnt working, what stim this?

what about H uniport

Back 54

Type II RTA, ANG II

Type I RTA, ALDO

Front 55

whats the deal in type IV RTA

Back 55

cant secrete NH4

**typically a result of hyperkalemia

**ALDO deficiency causes the hyperkalemia


**inhibits enzymes that degrade glutamine, GLutamine is our precursor for NH4

Front 56

what happens if you cant degrade glutamine

Back 56

cant make NH4, acidosis!


Glut is a way to handle chronic acid loads, if you no longer deal your acidictic

**seen in Type 4 RTA

Front 57

ok so correction...

when acidosis is due to HCO3 loss is the anion gap altered

Back 57

NOPE!

(we also increase Cl so the gap is the same)

**if however we have acidosis due to increased fixed acid loads bc Cl doesnt increase

Front 58

why is htere no change in the anion gap when acidosis is due to simple HCO3 loss

Back 58

be cl is increased

**increase in CL not seen when acidosis is due to increase in fixed acid

Front 59

disorders that increase the anion gap do what?

Back 59

increase fixed acid (lactate, oxalic acid), this decreased HCO3 w/o an increase in Cl

Front 60

what are 6 things that will increase the anion gap. fixed acid is increased, this decreases HCO3 with NO compensation of increased Cl

Back 60

1. lactic acidosis

2. Ketoacidosis (acettoacetic acid)

3. renal failure (accumulation of metabolic acids, pi adn sulfuric)

4. Asprin poisioning (salicylate poision)

5. Ethylene glycol poisioning: glycolic acid, oxalic acid

6. Metanol: formic acid

Anion Gap: Na - (HCO3 + Cl)

Normal gap is 8-16

Front 61

we know respiratory alkalosis is due to decreased CO2, name 3 reasons that Co2 might decrease

Back 61

1. stress, hypervent
2. altitude, hypervent
3. hypoxemia, hypervent

**lack of O2 in hypoxemia can lead to lactic acid production, helps combat the alkalosis

Front 62

so if you hypervent bc you are hypoxemic. how does the normal physio help itsself

Back 62

no O2, use aeribic respiration and make some lactic acid that will help redice the alkalosis that is seen

Front 63

so respiratoy acidosis occurs when we arent breathing enough and CO2 accumulates. name 4 instances when this happens

Back 63

-impairment of central respiratory regulation
–chest wall dysfunction
–impaired airway mechanics: COPD, obstruction
–impaired gas exchange

Front 64

what is normal plasma osM
is urine OSM more or less

can this be altered

Back 64

285-295
more (hyperosmotic)

YES! urine is a great way to maintain the plasma OSM bc the urine can be conc or dilute depending on the bodies needs

Front 65

what allows the urine to be both dilute and conc

Back 65

water and solute excretion are controlled independently

WAter: ADH
Na: AlDO

Front 66

in the LOH is more water or na reabs

in the DCT and CD is more water or Na rebs

Back 66

NA

Water

Front 67

where does most reabs occur

Back 67

PCT

Front 68

what hormone controls water? Na?

Back 68

Water: ADH
Na: ALDO

**independent regulation allows for conc and dilute urine formation

Front 69

of Na and H2O who is reabs passive? active? hormones

Back 69

Active: na adn water PASSIVELY follows

Water: ADH
Na: ALDO

Front 70

the countercurrent multiplier is made by who? who uses it?

Back 70

made by LOH
Used by CD

Front 71

in teh LOH we reans more _ than _____

Back 71

salt, water

Front 72

the CCM creates a large gradient from the __ to the ____ by multiplying ___ by __

Back 72

where the cortex and medulla meet
papila

conc difference
length of the multiplier

Front 73

what happens to the fluid in the LOH as it descends? ascends?

Back 73

Descends: concentrated
Ascedns: diluted

Front 74

what is the largest conc difference that is maintained in the ascending limb

Back 74

200 mOSm

Front 75

the osmotic gradient is set up where in the kidney? what does it do?

Back 75

in the medulla

**used to remove H2O from the urine in the CD, make a concentrated urine

Front 76

what is the "diluting segemnt" of the LOH

Back 76

ascending limb, pumps ions out, water cant follow

*impermiabel to water

Front 77

what part of LOH is impermiable to water? what happens here

Back 77

ascending

**reabs NaCL, this makes the fluid in the lumen dilute

Front 78

what allows dilute urine formation

Back 78

the ascending limb of LOH is where NaCl is reabs, water CANT follow here. this makes the urine in the lumen dilute

Front 79

what does the descending limb do? ascending

Back 79

descending: Water leaved the lumen and Nacl is Trapped (makes the lumen concentrated)

Ascending: Nacl is reabs and h2o is stuck! makes the urine dilute

**keep in mind overall in the LOH more Na is reabs than H20

Front 80

what limb concentrates the content of the lumen, how

Back 80

descending. H2o is permiable and leaves, NaCL stays put!

Front 81

what does it mean that the counter- current multiplier takes a small local current and multiplies it by the length of the multiplier? what does the 'counter" refer to

Back 81

well we know the max osm gradient can only be 200, but as we descend through the medulla we can get SUPER conc, this is because we multiply the 200 times the length as we go deeper into the medulla

counter bc flow is in the opposite direction in the 2 limbs

Front 82

if active transport was inhiibited could we have the countercurrent multiplier?

Back 82

nope! its KEY

**NaCL is actively transported in the descending limb

Front 83

where does NaCl reabs take place? how?

Back 83

ascending limb

**Na/K/2Cl transporter brings ions into the tubule and then they leave the basolateral mambrane by 1. Na/K and 2. K/Cl ssynport

Front 84

how does Na/Cl enter the tubule cell for reabs inthe ascending LOH

can this process be inhibited? stimulated

Back 84

Na/K/2Cl

inhibited by florosemide, loop diuretic

activated by ADH

Front 85

so NaCl is reabs in the ascending limb, and we know it enters the tubule via Na/K/2Cl. how does it leave the cell

Back 85

1. Na/K antiport
2. K/Cl synport

Front 86

how do we inhibit the Na/K/2Cl? how do we stim? what is this transporter involved in

Back 86

loop diuretics, furosemide
ADH
reabs of NaCl in the ascending limb

Front 87

why doesnt renal BF wash away the solutes in teh medulla ISF and take away the conc grad

Back 87

countercurrent exchange by the vasarecta protects the corticomedullary gradient

**as blood flows down the capillary NaCl enters and H2O moves out

Front 88

what is the goal of the desceniding limb?

Back 88

water leaves the tubule and enters the ISF

**the Vasa recta at this point is abs NaCl adn water is leaking out

**lots of H2O is entering the ISF

Front 89

what makes up most of the osmolites in the medulla

Back 89

urea

Front 90

what does a high protein diet do to ability to conc urine

Back 90

increased ability!

protein --> urea, urea is what makes the conc gradient in the medulla

Front 91

what areas of the nephron are imperm to urea? urea moves from where to where

Back 91

thick ascending limb and DCT are imperm to urea

**urea leaves at the CD and enters at the bottom of the LOH

Front 92

urea does what to the ISF osm? what fx does this serve

Back 92

increases the osm

*concentrates the fluids in the collecting duct

Front 93

what is urea recycling?

Back 93

urea enters the tubule at the tip of LOH. it then leaves at the distal CD

Front 94

how is permiability of urea to the CD in the inner medulla increased

Back 94

ADH

Front 95

is the Na/K/2Cl present in the early DCT

Back 95

nope

It has a Na/Cl symport that is sensitive to thiazide diuretics

Front 96

what does hte early DCT do

Back 96

reabs NaCl (same as descending)

Front 97

where do thiazide diuretics work

Back 97

on the Na/Cl symport in the early DCT

**cant reabs Na, so cant reabs H2O

Front 98

what transporter allows NaCl reabs in the ealy DC

Back 98

Na/Cl symport

**sensitive to thiazide diuretics

Front 99

what does chlorothiazide do? where does it work>

Back 99

blocks Na/Cl reabs in the early DCT

**this prevents H2O reabs and you pee lots!

Front 100

is the early DCT permiable to water

Back 100

nope

**diluting segment

Front 101

what is the diluting segemnt of the nephrin

Back 101

early DCT, NaCl reabs and NOT permiable to H2O

Front 102

where are the a intercalated and principal cells

Back 102

DCT (late)