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29 Cards in this Set
- Front
- Back
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. |
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 |
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Renal tubular acidoses, both distal and proximal
1)Do they cause anion Gap? 2) They cause ___2____ chloremia |
1)
2) Hyperchloremia |
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proximal RTA is a defect in reabsorption of?
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HCO3-
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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____ |
1) protein
2) Mitochondropathy 3) Fanconi's 4) Basal Na+/HCO3- transporter 5) Carbonic Anhydrase 6) Acetazolamide 7) Reduce IOP in glaucoma |
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pRTA
1) typical range of HCO3- 2) Is Urine pH high or low? 3) ____kalemia, why? |
1) 14-20
2) low = <5.5 3) hyperkalemia, because of less proximal reabsorbtion and more distal secretion due to increased Na+ presnentation |
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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___
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1) rickets
2) osteomalacia 3) Ca++ 4) D3 5) PTC |
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1) treatment of pRTA
2) problem with this |
1) IV NaHCO3 or K-Citrate (precursor of Bicarb)
2) Rapidly wasted as soon as it exceeds tubular maximum. |
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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...... |
1)H+
2) Alpha-interclated 3) hypokalmeia 4) type I |
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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___. |
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 |
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1) What makes a dRTA is
"classic" 2) classic dRTA has _____kalemia 3) causes risk of ______ 4) associated with ___ urine pH |
1) defect in alpha intercalated cells of C and MCD
2) hypo 3) kidney stones 4) high (alkline) |
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How does dRTA cause kidney stones
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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.
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Why do pRTA patients not form stones while dRTA patients do?
1) pH 2) wasting of 2 substances |
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. |
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Treatment of hypokalemic dRTA reqires more/less alkali upplemetation than pRTA
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much less
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There are two causes of dRTA which can cause HYPERkalemia
1) Involves principle cells of the CCD 2) Sick Collecting duct syndrome |
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 |
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Causes of HYPERkalemic dRTAs
1) Primary reduced Na+ transport 2) Sick CD syndrome 3) Summary of what must be compromised in general |
1) aldo deficiency
ACE-inhibitors Reduced distal Na+ presentation 2) Obstruction sickle cell acute interstital nephritis 3) pical Na+/K+ "exchange" |
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Tx of HYPERkalemis dRTA
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dietary K restricton
Na/K exchange resin (Kaexylate) Loop diuretic with Na+ replacement |
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Prevalence:
1) pRTA 2) classical dRTA (hypokalemic) 3) Hyperkalemic dRTA (type 4) 4) Hyperkalemic dRTA (sick C and MCD) |
1) rare
2) rare 3) very common 4) common |
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Plasma K+
1) pRTA 2) classical dRTA (hypokalemic) 3) Hyperkalemic dRTA (type 4) 4) Hyperkalemic dRTA (sick C and MCD) |
1) low
2) low 3) high 4) high |
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Urine pH
1) pRTA 2) classical dRTA (hypokalemic) 3) Hyperkalemic dRTA (type 4) 4) Hyperkalemic dRTA (sick C and MCD) |
1) <5.5
2) >6 3) <5.5 4) variable |
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Urine NH4+
1) pRTA 2) classical dRTA (hypokalemic) 3) Hyperkalemic dRTA (type 4) 4) Hyperkalemic dRTA (sick C and MCD) |
1)Normal
2)low 3) low 4) low |
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defect
1) pRTA 2) classical dRTA (hypokalemic) 3) Hyperkalemic dRTA (type 4) 4) Hyperkalemic dRTA (sick C and MCD) |
1) decreased HCO3 transport
2) Decreased H+ secretion 3) Decreased ammoniagenesis, decreased aldo effect 4) decreased Distal Na+ trasport |
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Rx
1) pRTA 2) classical dRTA (hypokalemic) 3) Hyperkalemic dRTA (type 4) 4) Hyperkalemic dRTA (sick C and MCD) |
1) HCO3-
2) CHO3- 3) Loop Diuretics 4) HCO3- |
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Example
1) pRTA 2) classical dRTA (hypokalemic) 3) Hyperkalemic dRTA (type 4) 4) Hyperkalemic dRTA (sick C and MCD) |
1) Acetazolamide
2) amphotericin 3) Diabetes 4) Obstruction |
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How do RTAs cause decreased excitation contraction coupling?
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By wasting Ca++ they draw Ca++ out of intracellular stores--- causes muscle weakness
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Uremic acidosis is caused by? (VERY general)
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renal failure
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1) Does uremic acidosis cause an Anion gap?
2) why? |
1) YES
2) SO4 an HPO4 (2-) are not well filtered when GFR drops |
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1) Uremic acidosis causes PO4- retention, what is a downstream effect of this initally?
2) How does this change with time? |
1) Increased PTH intitially to halt renal PO4 reabsorbtion.
2) this is overwhelmed and PO4 overload exacerbates |
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How does the kidney compensate for dietary K+ restriction? How does this cause a mild change in acid base status?
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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.
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Two coupled events which help the kidney waste excess Ca++ without causing stones to ppt.
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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> |