Renal: Electrolyte Wrap-Up

Front 1

Name two things that can cause decoupling of ADH from AQP insertion, resulting in a nephrogenic D.I.
1) A drug
2) An ionic state

3) Amphotericin B is another drug which can cause nephrogenic D.I. acts by putting a ___3___ permeable channel in the ___4_____. This allows leak of ___5___, reducing the activity of the ___5____ sensitive ____6______. This effect of Amphotericin B can be mimiced by chronic ___7__ kalemia.

Back 1

1) Lithium inhibits cAMP production
2) Hypercalcemia causes cAMP to be degraded more rapidly
3) cation
4) C and MCD
5) K+
6) Adenylate Cyclase
7) Hypokalemia

Front 2

Renal tubular acidoses, both distal and proximal
1)Do they cause anion Gap?
2) They cause ___2____ chloremia

Back 2

1)
2) Hyperchloremia

Front 3

proximal RTA is a defect in reabsorption of?

Back 3

HCO3-

Front 4

pRTA can result from
1) toxicity of ______ overload
2) ________pathy
3) _______'s Syndrome
4) hereditary defect in.....
5) Drug induced defect in brush border _____5______ cause.
6-7) ___6___ if the drug that causes (5), it is given for ____7____

Back 4

1) protein
2) Mitochondropathy
3) Fanconi's
4) Basal Na+/HCO3- transporter
5) Carbonic Anhydrase
6) Acetazolamide
7) Reduce IOP in glaucoma

Front 5

pRTA
1) typical range of HCO3-
2) Is Urine pH high or low?
3) ____kalemia, why?

Back 5

1) 14-20
2) low = <5.5
3) hyperkalemia, because of less proximal reabsorbtion and more distal secretion due to increased Na+ presnentation

Front 6

If untreated pRTA ca lead to ___1___ in children or ___2_____ in adults due to increased H+/___3____ exchange and ecreased secretion of ___4____ by the __5___

Back 6

1) rickets
2) osteomalacia
3) Ca++
4) D3
5) PTC

Front 7

1) treatment of pRTA
2) problem with this

Back 7

1) IV NaHCO3 or K-Citrate (precursor of Bicarb)
2) Rapidly wasted as soon as it exceeds tubular maximum.

Front 8

1) dRTA is a result of inability of the distal tubule to secrete ______
2) When dRTA is a genetic defect in the _____2_____ cells, it also presents with _____3____kalemia
4) This genetic dRTA is called type......

Back 8

1)H+
2) Alpha-interclated
3) hypokalmeia
4) type I

Front 9

Causes of dRTA
1) defective basolateral ____1____ transporters also known as ____2___ in erythrocytes.
3) (1) is associated with what other symptom?
4) Defective cytoplasmic ____4_____ (enzyme)
5-6) Defective apical _____5____ or ___6____
7) Because these two transporters (5-6) are critical in osteoclasts, this defect is also associated with ______7____ disorders
8) defective basolateral ____8____ cotransporters. This can cause reduced delivery of titratable buffers to the tubular lumen as is associted with defects of the ____9___.

Back 9

1) HCO3-/Cl-
2) Band 3
3) Hemolytic anemia
4)Carbonic anhydrase
5) H/K ATPase
6) H+ ATPase
7) Bone.growth disorders
8) K/Cl co-transporters
9) cochlea

Front 10

1) What makes a dRTA is
"classic"
2) classic dRTA has _____kalemia
3) causes risk of ______
4) associated with ___ urine pH

Back 10

1) defect in alpha intercalated cells of C and MCD
2) hypo
3) kidney stones
4) high (alkline)

Front 11

How does dRTA cause kidney stones

Back 11

1) inability to secrete H+ leads to reclamation of bicarb precursor. Citrate ususally binds Ca++ to make soluble complexes, but in its absence, Ca++ binds Phosphate (HPO42-) or oxalate whih can precipitates especially at this high pH.

Front 12

Why do pRTA patients not form stones while dRTA patients do?
1) pH
2) wasting of 2 substances

Back 12

pRTA has low urinary pH which pushes HPO4(2-) --> H2PO4 (1-) THis increases the solubility of the resulting Ca++ complex
2) wasting of AA and citrate which complex with Ca++ to form insoluble complexes.

Front 13

Treatment of hypokalemic dRTA reqires more/less alkali upplemetation than pRTA

Back 13

much less

Front 14

There are two causes of dRTA which can cause HYPERkalemia
1) Involves principle cells of the CCD
2) Sick Collecting duct syndrome

Back 14

1) CCD principle cells have reduced Na+ reabsorption, leading to lots of K+ reabsorbtion.
2) CANT reabsorb Na+ so the TEP which drive K+ secretion is gone

Front 15

Causes of HYPERkalemic dRTAs
1) Primary reduced Na+ transport
2) Sick CD syndrome
3) Summary of what must be compromised in general

Back 15

1) aldo deficiency
ACE-inhibitors
Reduced distal Na+ presentation
2) Obstruction
sickle cell
acute interstital nephritis
3) pical Na+/K+ "exchange"

Front 16

Tx of HYPERkalemis dRTA

Back 16

dietary K restricton
Na/K exchange resin (Kaexylate)
Loop diuretic with Na+ replacement

Front 17

Prevalence:
1) pRTA
2) classical dRTA (hypokalemic)
3) Hyperkalemic dRTA (type 4)
4) Hyperkalemic dRTA (sick C and MCD)

Back 17

1) rare
2) rare
3) very common
4) common

Front 18

Plasma K+
1) pRTA
2) classical dRTA (hypokalemic)
3) Hyperkalemic dRTA (type 4)
4) Hyperkalemic dRTA (sick C and MCD)

Back 18

1) low
2) low
3) high
4) high

Front 19

Urine pH
1) pRTA
2) classical dRTA (hypokalemic)
3) Hyperkalemic dRTA (type 4)
4) Hyperkalemic dRTA (sick C and MCD)

Back 19

1) <5.5
2) >6
3) <5.5
4) variable

Front 20

Urine NH4+
1) pRTA
2) classical dRTA (hypokalemic)
3) Hyperkalemic dRTA (type 4)
4) Hyperkalemic dRTA (sick C and MCD)

Back 20

1)Normal
2)low
3) low
4) low

Front 21

defect
1) pRTA
2) classical dRTA (hypokalemic)
3) Hyperkalemic dRTA (type 4)
4) Hyperkalemic dRTA (sick C and MCD)

Back 21

1) decreased HCO3 transport
2) Decreased H+ secretion
3) Decreased ammoniagenesis, decreased aldo effect
4) decreased Distal Na+ trasport

Front 22

Rx
1) pRTA
2) classical dRTA (hypokalemic)
3) Hyperkalemic dRTA (type 4)
4) Hyperkalemic dRTA (sick C and MCD)

Back 22

1) HCO3-
2) CHO3-
3) Loop Diuretics
4) HCO3-

Front 23

Example
1) pRTA
2) classical dRTA (hypokalemic)
3) Hyperkalemic dRTA (type 4)
4) Hyperkalemic dRTA (sick C and MCD)

Back 23

1) Acetazolamide
2) amphotericin
3) Diabetes
4) Obstruction

Front 24

How do RTAs cause decreased excitation contraction coupling?

Back 24

By wasting Ca++ they draw Ca++ out of intracellular stores--- causes muscle weakness

Front 25

Uremic acidosis is caused by? (VERY general)

Back 25

renal failure

Front 26

1) Does uremic acidosis cause an Anion gap?
2) why?

Back 26

1) YES
2) SO4 an HPO4 (2-) are not well filtered when GFR drops

Front 27

1) Uremic acidosis causes PO4- retention, what is a downstream effect of this initally?
2) How does this change with time?

Back 27

1) Increased PTH intitially to halt renal PO4 reabsorbtion.
2) this is overwhelmed and PO4 overload exacerbates

Front 28

How does the kidney compensate for dietary K+ restriction? How does this cause a mild change in acid base status?

Back 28

type A interclated cells xpress a apical H/K ATPase (EXCHANGER). This can act to reaborb almost all urinary K+ with the secretion of acid (causing a mild alkalosis). These cells are upregulated during hypokalemia.

Front 29

Two coupled events which help the kidney waste excess Ca++ without causing stones to ppt.

Back 29

1) TALH has a CA++ GPCR wich can inhibit Na/K/2Cl transport in the PCT, thus abolishing the TEP for Ca++ reabsorption.
2) Ca++ binding of GPCR in the nephron inhibits ADH action in the C and MCD, causing water wasting as well to dilute out the high urinary Ca++.

NET = CALCIURESIS IN DILUTE URINE>