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Potassium Disorders
         Alon Antebi MD
 The Institution for Nephrology &
           Hypertension
      Carmel Medical Center
Distribution of potassium between
          the cells and ECF
►The  total body K+ stores: 3000-4000 meq
►98% ICF
►ICF: 140meqL
►ECF: 4-5meqL
►Kept by NaK ATPase
FUNCTIONS OF POTASSIUM
►participatingin the regulation of such
 processes as protein and glycogen synthesis

►determinant  of the resting membrane
 potential (Em) across the cell membrane
Transcellular Potassium Gradient


     Na+    Intracellular K+:
            120-150 mmol/L
                           2 K+

           K+                            3 Na+

                EM = -90 mV       Extracellular K+:
                                   3.5-5.0 mmol/L
►Thus, both hypokalemia and hyperkalemia
 can result in potentially fatal muscle
 paralysis and cardiac arrhythmias

►the movement of as little as 1.5 to 2 percent
 of the cell K+ into the ECF can result in a
 potentially fatal increase in the plasma K+
 concentration to as high as 8 meq/L or more
Distribution of potassium
 between the cells and
           ECF
Potassium Homeostasis

 Intake




                            K +
                 Internal
                 Balance
   K+
3.5-5.0 mmol/L


          ECF

                            120-150 mmol/L


Excretion
                                ICF
3 Glasses of Orange
        Juice
3 Glasses of Orange
        Juice
  =40meq of K+
3 Glasses of Orange   ► 70   Kg
        Juice
  =40meq of K+
3 Glasses of Orange   ► 70Kg
        Juice         ► TBW=0.6 *BW=42L
  =40meq of K+
3 Glasses of Orange   ► 70Kg
        Juice         ► TBW=0.6 *BW=42L
  =40meq of K+        ► ECF= 0.33*TBW=14L
3 Glasses of Orange   ► 70Kg
        Juice         ► TBW=0.6 *BW=42L
  =40meq of K+        ► ECF= 0.33*TBW=14L
                      ► 40meq14L= 2.8meql
3 Glasses of Orange   ► 70 Kg
        Juice         ► TBW=0.6 *BW=42L
  =40meq of K+        ► ECF= 0.33*TBW=14L
                      ► 40meq14L= 2.8meql
                      ► 4.5+2.8=7.3meqL
3 Glasses of Orange   ► 70  Kg
        Juice         ► TBW=0.6 *BW=42L
  =40meq of K+        ► ECF= 0.33*TBW=14L
                      ► 40meq14L= 2.8meql
                      ► 4.5+2.8=7.3meqL
                      ► !!!!!!!
3 Glasses of Orange   ► 70  Kg
        Juice         ► TBW=0.6 *BW=42L
  =40meq of K+        ► ECF= 0.33*TBW=14L
                      ► 40meq14L= 2.8meql
                      ► 4.5+2.8=7.3meqL
                      ► !!!!!!!
                      ► ????
Sodium-potassium-ATPase
►The   activity of this pump is regulated by:
  Catecholamines
  Insulin
  the state of K+ balance
  thyroid hormone
  PH
Catecholamines
► alpha-receptors impairing and ß2-
  receptors promoting the cellular entry of K
  +
► ß-adrenergic blocker can aggravate
  hyperkalemia
► stress response –
       release of epinephrine
       rise in insulin release
►Insulin
►Insulin
►K+   loading
►Insulin
►K+ loading
►Exercise induced
►Insulin
►K+ loading
►Exercise induced
►PH
HYPEROSMOLALITY
►Creation   of K gradient due to water shift out
 of cells
►Solvant drag
Rate of cell breakdown and
             production
►Breakdown:
  Severe trauma
  Tumor lysis syndrome
  Rhabdomyolysis
►Production:
  Treated megaloblastic anemia with B12 or F.A.
Renal potassium
   excretion
►Kidney   handles about 90-95% of K+ daily
 load
►normal range is 40 to 120 meq/day
►tubular cell in the distal nephron:
   Principal cells
   Intercalated cells
►Almost all of the filtered K+ is reabsorbed in
 the proximal tubule and the loop of Henle

►less than 10% of the filtered load is
 delivered to the early distal tubule
Controling k+ handling by kidney
Controling k+ handling by kidney
►Aldosterone
  Na-K ATPase
  Na channels (Amiloride)
Controling k+ handling by kidney
►Aldosterone
  Na-K ATPase
  Na channels (Amiloride)
►Plasma   K+ concentration
Controling k+ handling by kidney
►Aldosterone
   Na-K ATPase
   Na channels (Amiloride)
►Plasma  K+ concentration
►The flow rate to the distal nephron (Distal
 Delivery
   Non Reabsorable Anions
Controling k+ handling by kidney
►Aldosterone
   Na-K ATPase
   Na channels (Amiloride)
►Plasma  K+ concentration
►The flow rate to the distal nephron (Distal
 Delivery
   Non Reabsorable Anions
►Obligatory   loss of 5 to 15 meq/day
Hypokalemia - I [DD]


►Intake                    ► Shifts
   diet                       Insulin administration
►Extrarenal    potassium       Catecholamine excess
 loss                          Drugs
   diarrhea                   Familial periodic
                                hypokalemic paralysis
►Urinary   losses              Thyrotoxic hypokalemic
   diuretics [loop,            paralysis
    thiazides]                 ALKAOSIS
   vomiting
Hypokalemia – URINARY
             LOSS: Uk>20meqL

►Hypokalemia   without HTN   ► Hypokalemia   with HTN
  Distal RTA [Type 1]          Renin secretion states
  Proximal RTA [Type 2]        Renovascular
  Amphotericin B                Hypertension
  Bartter’s Syndrome           Primary Hyper-ALDO
  Gittelman’s Syndrome         Malignant Hypertension
                                GRA
  Hypomagnesemia
                                AME
  Diuretics
                                Liddle’s syndrome
  Vomiting
  NRA
EKG Manifestations of
                          Hypokalemia
                                Normal
Decreasing Serum K+




                                Flat T-wave


                                Prominent U-wave


                                Depressed ST-segment
TREATMENT
TREATMENT
►K+   supplementation
  small doses, frequent checks
  P.O.
      ►safer,   20 - 40 meq per day
  I.V.
      ►reserve   for severe symptomatic cases [<3.0
       meq/L]
      ►reserve for patients without P.O. possibility
      ►check Plasma Potassium every 2- 3 hours
      ►continuous ECG monitoring
TREATMENT
►K+   supplementation
  small doses, frequent checks
  P.O.
      ►safer,   20 - 40 meq per day
  I.V.
      ►reserve   for severe symptomatic cases [<3.0
       meq/L]
      ►reserve for patients without P.O. possibility
      ►check Plasma Potassium every 2- 3 hours
      ►continuous ECG monitoring

►Correct    underlying cause
TREATMENT
►K+   supplementation
  small doses, frequent checks
  P.O.
      ►safer,   20 - 40 meq per day
  I.V.
      ►reserve   for severe symptomatic cases [<3.0
       meq/L]
      ►reserve for patients without P.O. possibility
      ►check Plasma Potassium every 2- 3 hours
      ►continuous ECG monitoring

►Correctunderlying cause
►Asses and correct Hypomagnesemia
Hyperkalemia - I [DD]

►Pseudohyperkalemia ► Abnormal      distribution
  Hemolysis [pink      Insulin Deficiency
   serum]               Beta-blockers
  Thrombocytosis       Metabolic Acidosis
  Leukocytosis      ► Abnormal     Release
  Fist clenching      from cells
  Tourniqueting        Rhabdomyolysis
                        Tumor Lysis
                         Syndrome
Hyperkalemia - II [DD]

►Decreased   Renal Excretion
  Acute or Chronic Renal failure
  ALDO deficiency [Type IV RTA]- rare
  Drug Induced: ACE INH, ALDACTON
  Kidney disease impairing distal tubular function
   or filtration
HYPOALDOSTERONISM

  ►Hyporenin-hypoaldo   with CKD
  ►NSAID’S
  ►ACE-I/ARB
  ►CYCLOSPORINE
  ►AMILORIDE/TRIAMTERENE
  ►ALDACTONE
  ►ADRENAL INSUFFICIENCY
  ►HEPARIN
Diet
EKG Manifestations of
                         Hyperkalemia
                                Normal
Increasing Serum K+




                                Peaked T-wave

                                Wide QRS Complex
                                Prolonged PR Interval

                                Further Widening of QRS Complex
                                Absent P-Wave

                                Sine Wave
TREATMENT
TREATMENT

►Stabilize   myocardium
   I.V. bolus 10 ml 10% CaGluconate or CaCl2 [over 1 minute], if
    no response in 3-5 minutes repeat the dose
   This does not lower K level !!!!!!!!
TREATMENT

►Stabilize   myocardium
   I.V. bolus 10 ml 10% CaGluconate or CaCl2 [over 1 minute], if
    no response in 3-5 minutes repeat the dose
   This does not lower K level !!!!!!!!
►Monitor     ECG
TREATMENT

►Stabilize   myocardium
   I.V. bolus 10 ml 10% CaGluconate or CaCl2 [over 1 minute], if
    no response in 3-5 minutes repeat the dose
   This does not lower K level !!!!!!!!
►Monitor     ECG
►Shift   Potassium
   I.V. Insulin 10U + 50ml D50W [works in 15 minutes]
   follow by I.V. D5W 100ml/h
   Inh. 20mg Albuterol over 10 minutes [works in 30 minutes]
   I.V. 0.5 mg Albuterol
►Diuretics
  type
  renal function?
►Kaexalate   (Na Polystyrene)
  30 to 50 gram
  each gram removes 1meq K+
  retention enema (give with 50 ml sorbitol)
►Diuretics
   type
   renal function?
►Kaexalate   (Na Polystyrene)
   30 to 50 gram
   each gram removes 1meq K+
   retention enema (give with 50 ml sorbitol)
►Dialysis
EXERCISE 1
►47 Years old woman is hospitelised because
 of Acute Cholecystitis
►She is getting Abx & IV Saline 0.9%, Gastric
 Tube
►You are called on the third day of treatment
 because of:
►Na=139 K=2.8 Cl=85 (95-105)
►PH=7.59, PCO2=57 PO2=92, HCO3=46
EXERCISE 2
►19 Years old soldier arrives in the ER
 because of weakness
►She weights 40Kg, BP= 110/70
►K=2
►Na=140
►Cr=0.9
►Glu= 90
►Ca=8.9
►PH=7.50
►HCO3=32
►PCO2=46
►PH=7.50
►HCO3=32
►PCO2=46
►Urine   Electrolytes: Na=40 K=40 Cl=50
►What is the DD?
►Does she take Laxatives?
►How can you convince the psychiatrist to
 examine her?

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Icm k disorders 194

  • 1. Potassium Disorders Alon Antebi MD The Institution for Nephrology & Hypertension Carmel Medical Center
  • 2. Distribution of potassium between the cells and ECF ►The total body K+ stores: 3000-4000 meq ►98% ICF ►ICF: 140meqL ►ECF: 4-5meqL ►Kept by NaK ATPase
  • 3. FUNCTIONS OF POTASSIUM ►participatingin the regulation of such processes as protein and glycogen synthesis ►determinant of the resting membrane potential (Em) across the cell membrane
  • 4. Transcellular Potassium Gradient Na+ Intracellular K+: 120-150 mmol/L 2 K+ K+ 3 Na+ EM = -90 mV Extracellular K+: 3.5-5.0 mmol/L
  • 5. ►Thus, both hypokalemia and hyperkalemia can result in potentially fatal muscle paralysis and cardiac arrhythmias ►the movement of as little as 1.5 to 2 percent of the cell K+ into the ECF can result in a potentially fatal increase in the plasma K+ concentration to as high as 8 meq/L or more
  • 6.
  • 7. Distribution of potassium between the cells and ECF
  • 8. Potassium Homeostasis Intake K + Internal Balance K+ 3.5-5.0 mmol/L ECF 120-150 mmol/L Excretion ICF
  • 9.
  • 10.
  • 11.
  • 12. 3 Glasses of Orange Juice
  • 13. 3 Glasses of Orange Juice =40meq of K+
  • 14. 3 Glasses of Orange ► 70 Kg Juice =40meq of K+
  • 15. 3 Glasses of Orange ► 70Kg Juice ► TBW=0.6 *BW=42L =40meq of K+
  • 16. 3 Glasses of Orange ► 70Kg Juice ► TBW=0.6 *BW=42L =40meq of K+ ► ECF= 0.33*TBW=14L
  • 17. 3 Glasses of Orange ► 70Kg Juice ► TBW=0.6 *BW=42L =40meq of K+ ► ECF= 0.33*TBW=14L ► 40meq14L= 2.8meql
  • 18. 3 Glasses of Orange ► 70 Kg Juice ► TBW=0.6 *BW=42L =40meq of K+ ► ECF= 0.33*TBW=14L ► 40meq14L= 2.8meql ► 4.5+2.8=7.3meqL
  • 19. 3 Glasses of Orange ► 70 Kg Juice ► TBW=0.6 *BW=42L =40meq of K+ ► ECF= 0.33*TBW=14L ► 40meq14L= 2.8meql ► 4.5+2.8=7.3meqL ► !!!!!!!
  • 20. 3 Glasses of Orange ► 70 Kg Juice ► TBW=0.6 *BW=42L =40meq of K+ ► ECF= 0.33*TBW=14L ► 40meq14L= 2.8meql ► 4.5+2.8=7.3meqL ► !!!!!!! ► ????
  • 21. Sodium-potassium-ATPase ►The activity of this pump is regulated by: Catecholamines Insulin the state of K+ balance thyroid hormone PH
  • 22.
  • 23. Catecholamines ► alpha-receptors impairing and ß2- receptors promoting the cellular entry of K + ► ß-adrenergic blocker can aggravate hyperkalemia ► stress response –  release of epinephrine  rise in insulin release
  • 24.
  • 25.
  • 27. ►Insulin ►K+ loading
  • 30.
  • 31. HYPEROSMOLALITY ►Creation of K gradient due to water shift out of cells ►Solvant drag
  • 32. Rate of cell breakdown and production ►Breakdown: Severe trauma Tumor lysis syndrome Rhabdomyolysis ►Production: Treated megaloblastic anemia with B12 or F.A.
  • 33. Renal potassium excretion
  • 34. ►Kidney handles about 90-95% of K+ daily load ►normal range is 40 to 120 meq/day ►tubular cell in the distal nephron: Principal cells Intercalated cells
  • 35. ►Almost all of the filtered K+ is reabsorbed in the proximal tubule and the loop of Henle ►less than 10% of the filtered load is delivered to the early distal tubule
  • 36.
  • 37.
  • 38.
  • 39.
  • 40.
  • 41.
  • 42.
  • 43.
  • 45. Controling k+ handling by kidney ►Aldosterone Na-K ATPase Na channels (Amiloride)
  • 46. Controling k+ handling by kidney ►Aldosterone Na-K ATPase Na channels (Amiloride) ►Plasma K+ concentration
  • 47. Controling k+ handling by kidney ►Aldosterone Na-K ATPase Na channels (Amiloride) ►Plasma K+ concentration ►The flow rate to the distal nephron (Distal Delivery Non Reabsorable Anions
  • 48. Controling k+ handling by kidney ►Aldosterone Na-K ATPase Na channels (Amiloride) ►Plasma K+ concentration ►The flow rate to the distal nephron (Distal Delivery Non Reabsorable Anions ►Obligatory loss of 5 to 15 meq/day
  • 49.
  • 50.
  • 51.
  • 52. Hypokalemia - I [DD] ►Intake ► Shifts diet  Insulin administration ►Extrarenal potassium  Catecholamine excess loss  Drugs diarrhea  Familial periodic hypokalemic paralysis ►Urinary losses  Thyrotoxic hypokalemic diuretics [loop, paralysis thiazides]  ALKAOSIS vomiting
  • 53. Hypokalemia – URINARY LOSS: Uk>20meqL ►Hypokalemia without HTN ► Hypokalemia with HTN Distal RTA [Type 1]  Renin secretion states Proximal RTA [Type 2]  Renovascular Amphotericin B Hypertension Bartter’s Syndrome  Primary Hyper-ALDO Gittelman’s Syndrome  Malignant Hypertension  GRA Hypomagnesemia  AME Diuretics  Liddle’s syndrome Vomiting NRA
  • 54. EKG Manifestations of Hypokalemia Normal Decreasing Serum K+ Flat T-wave Prominent U-wave Depressed ST-segment
  • 55.
  • 57. TREATMENT ►K+ supplementation small doses, frequent checks P.O. ►safer, 20 - 40 meq per day I.V. ►reserve for severe symptomatic cases [<3.0 meq/L] ►reserve for patients without P.O. possibility ►check Plasma Potassium every 2- 3 hours ►continuous ECG monitoring
  • 58. TREATMENT ►K+ supplementation small doses, frequent checks P.O. ►safer, 20 - 40 meq per day I.V. ►reserve for severe symptomatic cases [<3.0 meq/L] ►reserve for patients without P.O. possibility ►check Plasma Potassium every 2- 3 hours ►continuous ECG monitoring ►Correct underlying cause
  • 59. TREATMENT ►K+ supplementation small doses, frequent checks P.O. ►safer, 20 - 40 meq per day I.V. ►reserve for severe symptomatic cases [<3.0 meq/L] ►reserve for patients without P.O. possibility ►check Plasma Potassium every 2- 3 hours ►continuous ECG monitoring ►Correctunderlying cause ►Asses and correct Hypomagnesemia
  • 60. Hyperkalemia - I [DD] ►Pseudohyperkalemia ► Abnormal distribution Hemolysis [pink  Insulin Deficiency serum]  Beta-blockers Thrombocytosis  Metabolic Acidosis Leukocytosis ► Abnormal Release Fist clenching from cells Tourniqueting  Rhabdomyolysis  Tumor Lysis Syndrome
  • 61. Hyperkalemia - II [DD] ►Decreased Renal Excretion Acute or Chronic Renal failure ALDO deficiency [Type IV RTA]- rare Drug Induced: ACE INH, ALDACTON Kidney disease impairing distal tubular function or filtration
  • 62. HYPOALDOSTERONISM ►Hyporenin-hypoaldo with CKD ►NSAID’S ►ACE-I/ARB ►CYCLOSPORINE ►AMILORIDE/TRIAMTERENE ►ALDACTONE ►ADRENAL INSUFFICIENCY ►HEPARIN
  • 63. Diet
  • 64. EKG Manifestations of Hyperkalemia Normal Increasing Serum K+ Peaked T-wave Wide QRS Complex Prolonged PR Interval Further Widening of QRS Complex Absent P-Wave Sine Wave
  • 65.
  • 67. TREATMENT ►Stabilize myocardium I.V. bolus 10 ml 10% CaGluconate or CaCl2 [over 1 minute], if no response in 3-5 minutes repeat the dose This does not lower K level !!!!!!!!
  • 68. TREATMENT ►Stabilize myocardium I.V. bolus 10 ml 10% CaGluconate or CaCl2 [over 1 minute], if no response in 3-5 minutes repeat the dose This does not lower K level !!!!!!!! ►Monitor ECG
  • 69. TREATMENT ►Stabilize myocardium I.V. bolus 10 ml 10% CaGluconate or CaCl2 [over 1 minute], if no response in 3-5 minutes repeat the dose This does not lower K level !!!!!!!! ►Monitor ECG ►Shift Potassium I.V. Insulin 10U + 50ml D50W [works in 15 minutes] follow by I.V. D5W 100ml/h Inh. 20mg Albuterol over 10 minutes [works in 30 minutes] I.V. 0.5 mg Albuterol
  • 70.
  • 71.
  • 72. ►Diuretics type renal function? ►Kaexalate (Na Polystyrene) 30 to 50 gram each gram removes 1meq K+ retention enema (give with 50 ml sorbitol)
  • 73. ►Diuretics type renal function? ►Kaexalate (Na Polystyrene) 30 to 50 gram each gram removes 1meq K+ retention enema (give with 50 ml sorbitol) ►Dialysis
  • 74. EXERCISE 1 ►47 Years old woman is hospitelised because of Acute Cholecystitis ►She is getting Abx & IV Saline 0.9%, Gastric Tube ►You are called on the third day of treatment because of: ►Na=139 K=2.8 Cl=85 (95-105) ►PH=7.59, PCO2=57 PO2=92, HCO3=46
  • 75. EXERCISE 2 ►19 Years old soldier arrives in the ER because of weakness ►She weights 40Kg, BP= 110/70 ►K=2 ►Na=140 ►Cr=0.9 ►Glu= 90 ►Ca=8.9
  • 76.
  • 77.
  • 79. ►PH=7.50 ►HCO3=32 ►PCO2=46 ►Urine Electrolytes: Na=40 K=40 Cl=50
  • 80. ►What is the DD? ►Does she take Laxatives? ►How can you convince the psychiatrist to examine her?

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  37. ascending loop of henle\n
  38. \n
  39. \nCD:\nprinciple cell \n\nsecrete k\n\n2 things control aldosterone in blood\n1) RAAS axis\n2) K levels\n- high aldosterone when: high levels of K/ low levels of blood flow\n\n\nactivate na/k atpase channel\nenac in luminal membrane- so na absorbed and k secreted\n- may control secretion of k in principle cell in cases of hyperkalemia\n\n\n\n
  40. CD:\n\nintercalated cell\n-type a) secrete h cations and absorb K\n- secrete protons and reabsorb bicarb\n-type b)\n\nprinciple secrete k, intercalated reabsorb k--- can control k levles in CD\n1) aldosterone levels affect it\n2) k level itself: if k is hgher than in the lumen- then will cause excretion of k into the lumen\n\nmin ways: aldosterone\n
  41. EBV low- glomer filtrate low, distal delivery low\n- high aldost bc of low distal delivery- but will have low distal secretion of k- cancel eachother and dont lose or add k\n\n\nhigh EBV\n- glomer high, distal delivery high\n- principle cell- low activation- low aldosterone (decreased)\n- so although much urine , low k, and low k secretion- dont lose or add k\n\nregularly you dont lose and you dont add more k then you need at the nephron\n-they cancel each other out\n- in normal status- will not add k to blood bc of kidney- will be normal\n\nso when do u have k problems?\n- when there is a problem here\nif both high or both low- will have problems\nexample\n- high level from tumor, high EBV- high distal delivery- but path excretion of k in distal nephron- bc of the hyperaldosteronism\n- high bp and hypokalemia\n\nCONTROL OF K\naldosterone level (direclty excreted by level of k and angiotensin\ndistal delivery of nephron\n\nhyperkalemic, with HTN- one ofthing that can happen when channel is disregulated: LIDDLE SYNDROME--disregulation of epith na \nchannel\n- amiloride- low bp- bc lose water bc of loww of na\n\nNON REABSORBABLE ANIONS\n- cases where na cant be reabsorbed in prox tubule bc anion that follows it cant be reabsorbed int he prox tubule\n- metabolic alkalosis (like in vomitting)\n- this extra bicarb usually excreted by filtration- kidey ty to get rid of it\n- na/bicarb get back- kideny want to get rid--- na and bicab not reabsorbed here-- distal delivery higher than distal nephron- bc of non reabsorbable anion\n- na drugs: much na inside- cant be reabsorbed bbc the anion part of the drug cant be reabsorbed- so the na ot reabsorbed either- they go with the water- go to distal nephrone- should be reabsorbed there- bc otherwise lose a lot fo na-- but in tis area, if na reabsorbed- need to be reabsorbed with something else- the cl- get rid of the carbopenems (the drug) -- low cl in urine, and will lose k bc of high level of distal delivery\n- so when pt vomit- lose k-- not by vomiting, but bc of increased distal delivery\n\nOBLIGATORY LOSS\nbc of gain btw principle cells and intercalated cells- cant absorb all of the k\n
  42. EBV low- glomer filtrate low, distal delivery low\n- high aldost bc of low distal delivery- but will have low distal secretion of k- cancel eachother and dont lose or add k\n\n\nhigh EBV\n- glomer high, distal delivery high\n- principle cell- low activation- low aldosterone (decreased)\n- so although much urine , low k, and low k secretion- dont lose or add k\n\nregularly you dont lose and you dont add more k then you need at the nephron\n-they cancel each other out\n- in normal status- will not add k to blood bc of kidney- will be normal\n\nso when do u have k problems?\n- when there is a problem here\nif both high or both low- will have problems\nexample\n- high level from tumor, high EBV- high distal delivery- but path excretion of k in distal nephron- bc of the hyperaldosteronism\n- high bp and hypokalemia\n\nCONTROL OF K\naldosterone level (direclty excreted by level of k and angiotensin\ndistal delivery of nephron\n\nhyperkalemic, with HTN- one ofthing that can happen when channel is disregulated: LIDDLE SYNDROME--disregulation of epith na \nchannel\n- amiloride- low bp- bc lose water bc of loww of na\n\nNON REABSORBABLE ANIONS\n- cases where na cant be reabsorbed in prox tubule bc anion that follows it cant be reabsorbed int he prox tubule\n- metabolic alkalosis (like in vomitting)\n- this extra bicarb usually excreted by filtration- kidey ty to get rid of it\n- na/bicarb get back- kideny want to get rid--- na and bicab not reabsorbed here-- distal delivery higher than distal nephron- bc of non reabsorbable anion\n- na drugs: much na inside- cant be reabsorbed bbc the anion part of the drug cant be reabsorbed- so the na ot reabsorbed either- they go with the water- go to distal nephrone- should be reabsorbed there- bc otherwise lose a lot fo na-- but in tis area, if na reabsorbed- need to be reabsorbed with something else- the cl- get rid of the carbopenems (the drug) -- low cl in urine, and will lose k bc of high level of distal delivery\n- so when pt vomit- lose k-- not by vomiting, but bc of increased distal delivery\n\nOBLIGATORY LOSS\nbc of gain btw principle cells and intercalated cells- cant absorb all of the k\n
  43. EBV low- glomer filtrate low, distal delivery low\n- high aldost bc of low distal delivery- but will have low distal secretion of k- cancel eachother and dont lose or add k\n\n\nhigh EBV\n- glomer high, distal delivery high\n- principle cell- low activation- low aldosterone (decreased)\n- so although much urine , low k, and low k secretion- dont lose or add k\n\nregularly you dont lose and you dont add more k then you need at the nephron\n-they cancel each other out\n- in normal status- will not add k to blood bc of kidney- will be normal\n\nso when do u have k problems?\n- when there is a problem here\nif both high or both low- will have problems\nexample\n- high level from tumor, high EBV- high distal delivery- but path excretion of k in distal nephron- bc of the hyperaldosteronism\n- high bp and hypokalemia\n\nCONTROL OF K\naldosterone level (direclty excreted by level of k and angiotensin\ndistal delivery of nephron\n\nhyperkalemic, with HTN- one ofthing that can happen when channel is disregulated: LIDDLE SYNDROME--disregulation of epith na \nchannel\n- amiloride- low bp- bc lose water bc of loww of na\n\nNON REABSORBABLE ANIONS\n- cases where na cant be reabsorbed in prox tubule bc anion that follows it cant be reabsorbed int he prox tubule\n- metabolic alkalosis (like in vomitting)\n- this extra bicarb usually excreted by filtration- kidey ty to get rid of it\n- na/bicarb get back- kideny want to get rid--- na and bicab not reabsorbed here-- distal delivery higher than distal nephron- bc of non reabsorbable anion\n- na drugs: much na inside- cant be reabsorbed bbc the anion part of the drug cant be reabsorbed- so the na ot reabsorbed either- they go with the water- go to distal nephrone- should be reabsorbed there- bc otherwise lose a lot fo na-- but in tis area, if na reabsorbed- need to be reabsorbed with something else- the cl- get rid of the carbopenems (the drug) -- low cl in urine, and will lose k bc of high level of distal delivery\n- so when pt vomit- lose k-- not by vomiting, but bc of increased distal delivery\n\nOBLIGATORY LOSS\nbc of gain btw principle cells and intercalated cells- cant absorb all of the k\n
  44. EBV low- glomer filtrate low, distal delivery low\n- high aldost bc of low distal delivery- but will have low distal secretion of k- cancel eachother and dont lose or add k\n\n\nhigh EBV\n- glomer high, distal delivery high\n- principle cell- low activation- low aldosterone (decreased)\n- so although much urine , low k, and low k secretion- dont lose or add k\n\nregularly you dont lose and you dont add more k then you need at the nephron\n-they cancel each other out\n- in normal status- will not add k to blood bc of kidney- will be normal\n\nso when do u have k problems?\n- when there is a problem here\nif both high or both low- will have problems\nexample\n- high level from tumor, high EBV- high distal delivery- but path excretion of k in distal nephron- bc of the hyperaldosteronism\n- high bp and hypokalemia\n\nCONTROL OF K\naldosterone level (direclty excreted by level of k and angiotensin\ndistal delivery of nephron\n\nhyperkalemic, with HTN- one ofthing that can happen when channel is disregulated: LIDDLE SYNDROME--disregulation of epith na \nchannel\n- amiloride- low bp- bc lose water bc of loww of na\n\nNON REABSORBABLE ANIONS\n- cases where na cant be reabsorbed in prox tubule bc anion that follows it cant be reabsorbed int he prox tubule\n- metabolic alkalosis (like in vomitting)\n- this extra bicarb usually excreted by filtration- kidey ty to get rid of it\n- na/bicarb get back- kideny want to get rid--- na and bicab not reabsorbed here-- distal delivery higher than distal nephron- bc of non reabsorbable anion\n- na drugs: much na inside- cant be reabsorbed bbc the anion part of the drug cant be reabsorbed- so the na ot reabsorbed either- they go with the water- go to distal nephrone- should be reabsorbed there- bc otherwise lose a lot fo na-- but in tis area, if na reabsorbed- need to be reabsorbed with something else- the cl- get rid of the carbopenems (the drug) -- low cl in urine, and will lose k bc of high level of distal delivery\n- so when pt vomit- lose k-- not by vomiting, but bc of increased distal delivery\n\nOBLIGATORY LOSS\nbc of gain btw principle cells and intercalated cells- cant absorb all of the k\n
  45. EBV low- glomer filtrate low, distal delivery low\n- high aldost bc of low distal delivery- but will have low distal secretion of k- cancel eachother and dont lose or add k\n\n\nhigh EBV\n- glomer high, distal delivery high\n- principle cell- low activation- low aldosterone (decreased)\n- so although much urine , low k, and low k secretion- dont lose or add k\n\nregularly you dont lose and you dont add more k then you need at the nephron\n-they cancel each other out\n- in normal status- will not add k to blood bc of kidney- will be normal\n\nso when do u have k problems?\n- when there is a problem here\nif both high or both low- will have problems\nexample\n- high level from tumor, high EBV- high distal delivery- but path excretion of k in distal nephron- bc of the hyperaldosteronism\n- high bp and hypokalemia\n\nCONTROL OF K\naldosterone level (direclty excreted by level of k and angiotensin\ndistal delivery of nephron\n\nhyperkalemic, with HTN- one ofthing that can happen when channel is disregulated: LIDDLE SYNDROME--disregulation of epith na \nchannel\n- amiloride- low bp- bc lose water bc of loww of na\n\nNON REABSORBABLE ANIONS\n- cases where na cant be reabsorbed in prox tubule bc anion that follows it cant be reabsorbed int he prox tubule\n- metabolic alkalosis (like in vomitting)\n- this extra bicarb usually excreted by filtration- kidey ty to get rid of it\n- na/bicarb get back- kideny want to get rid--- na and bicab not reabsorbed here-- distal delivery higher than distal nephron- bc of non reabsorbable anion\n- na drugs: much na inside- cant be reabsorbed bbc the anion part of the drug cant be reabsorbed- so the na ot reabsorbed either- they go with the water- go to distal nephrone- should be reabsorbed there- bc otherwise lose a lot fo na-- but in tis area, if na reabsorbed- need to be reabsorbed with something else- the cl- get rid of the carbopenems (the drug) -- low cl in urine, and will lose k bc of high level of distal delivery\n- so when pt vomit- lose k-- not by vomiting, but bc of increased distal delivery\n\nOBLIGATORY LOSS\nbc of gain btw principle cells and intercalated cells- cant absorb all of the k\n
  46. skip\n
  47. eat a lot of k\n\naldosterone\nurine k increase\nbut after 20 days, aldost level goes down, and if contnue eating the k- you dont get hyperkalemia- k level elevated slightly and will still be in normal levels\n- how does this happen? high level of aldost in beginning but then normalizes, and still dont get hyperkalemia\n- bc after 20 days- in luminal membrane have a lot of enac, -upregulation- secrete a lot of k even though aldost is low again-- dont elevate bp anymore, --can control the k level\n\n-can control k level unrelated to blood level- otherwise, anytime eat uch k, will be hypervolemic and high bp due to aldost\n- so initially high aldost, but then level out\n
  48. can cause hyperkalemia with these drugs\n- butdoesnt happen usually- why?\nbc although have low aldost activity- the bp high in beginning- high distal delivery- so dont cause hyperkalemia\n- when you do cause hyperkalemia- in case of low effective blood volume in addition to these drugs- acture kidney injury, dehydration\n---when low bp, or kidney injury or combo of diff drugs-- then can get hyperkalemic state\n
  49. block na/k/cl: barter syndrome\n- hypokalemic (lose k in distal bc of block of the transporter)\n- like furosemide\n\ngittleman- inactivation of na/k cotrasporter (sim to thiazide)\n- hypokalemia bc o renal excretion bc of the transporter\n\nin either situation: always excrete cl in urine-- dont absorb the cl and no roblem with non-reabsorbed aniona\n- so dd of lose k through kideny is based onthe cl level in the urine\n\n\ngittleman, barter, diuretics:\nhigh cl in urine\n\n\n\nhypokalemic pt\n- is kidney responsible or intake or shift?\n- take k level in urine\n-if high when pt hypokalemic- tehn means kidney not reabsorb the k even though hypokalmeic- the kidney is the problem\nhow know where the prob is in the kidney?:\nneed to know= 1) met alk/acidosis 9acid base status) 2) cl level in the urine (cl level)\n\n
  50. when normal bv-- aldosterone is not the problem- the problem is the distal delivery = high distal delivery\n\ndiarrhea: urinary k is low (bc kidney not responsible for this)\nplace where is responsible: renal tubular acidosis\n\nhigh urinary k level- kidney is the problem\nlow urinary k- the kidney is not the responsible one- diarrhea, low intake, or problem with shift (extracatechol, beta agonist...)\n\n\n\nurine cl low = non reabsorbed anions (vomit, or carbapenems- cant reabsorb the na proximally c of the anions- so absorbes distally withcl)\nurine cl is high = diuretics or barter or gittelman, or mg defficiency (hypokalemic pt with hypocalcemia- look for the mg levels- usually due to hypomagnesemia- need to correct the mg)\n\n\nHTN pt:\n- hypokalemia bc of kidney- main problem is hyperaldosterosism\n\nwhat can cause pathologically high aldost:\nA) high renin high aldost\n- renin secreting tumor\n- pt will have high renin and high aldost levels\n- renal artery stenosis- low effective blood to kidney\nB) low renin, high aldost- hyperaldosteronism, \nC) renin low, aldost low, but still high aldost activation of principlecell = \n- activation of enac\n- neg feedback of actiavtion of receptors for aldosterone- can be due to few path things\n- activation by cortisol- activate receptor of aldost\n- cortisol inactivated by enzyme- somtimes enzyme has genetic mutaiton or is inactivated by licorice-- not converted and can activate the receptor- high level cortisol- hypervolemic, high bp, aldost level suppressed- bc of high activation of receptor\n- hypokalemia- extra urinary excretion, high bp, low aldost: cushings syndrome, 11 beta defficiency or mutation or inactivation by licorice\n- hyper activation of receptor but renin and aldost are suppressed\n\nits either:\n1) renin or 2) aldosterone or 3) activation of receptor by something lese\n\n
  51. hypokalemia cause tachy\nhyperkalemia cause brady \n
  52. acid base balance NEEDED for dx\n-look at:\n1) acid base\n2) urinary electrolytes: k and cl\n3) bp\n
  53. acid base balance NEEDED for dx\n-look at:\n1) acid base\n2) urinary electrolytes: k and cl\n3) bp\n
  54. acid base balance NEEDED for dx\n-look at:\n1) acid base\n2) urinary electrolytes: k and cl\n3) bp\n
  55. acid base balance NEEDED for dx\n-look at:\n1) acid base\n2) urinary electrolytes: k and cl\n3) bp\n
  56. intake not usually effect- but if have other problems will (like if dont have kidney, or low effective blood volume- no filtration, no distal deli ery- no excretion)\n\n\neither extreme situation- ate so much k ( rare)\ndont have kidney (kidney failure) - most common\nhave kidney but fail bc of low ebv - most common\nor hypoaldosteronism (rare)\nsome drugs that block raas axis and cause low aldost - most common\n\n\nhigh k in lab- not really higjh k in blood\n- lab problem (hemolysis)\n.......\n\nmetabolic acidosis- shift of k from inside cells to outside\n\n
  57. \n
  58. heparin suppress aldost secretion from adrenal gland\n
  59. pts on dialysis shoulndt eat these\n
  60. \n
  61. \n
  62. \n
  63. \n
  64. \n
  65. not respond to dieretics, or kaexalate, or shit frombeta agonist.... = dialysis\n
  66. not respond to dieretics, or kaexalate, or shit frombeta agonist.... = dialysis\n
  67. not respond to dieretics, or kaexalate, or shit frombeta agonist.... = dialysis\n
  68. not respond to dieretics, or kaexalate, or shit frombeta agonist.... = dialysis\n
  69. not respond to dieretics, or kaexalate, or shit frombeta agonist.... = dialysis\n
  70. high pco2 \nhigh hco3\nhypokalemic\n\nhypokal\nalkylotic\nlow bp/normal bp\n\ngastric tube- doesnt absorb anything from the gastric outlet to the gut (similar to idea of vomitting)\n- metabolic alkalosis, kidney try to get rid of bicarb- non-absorb anion- high distal delivery- increased excretion of k\n\n- high urinary k\n- low urinary cl\n\n
  71. \n
  72. high ph\n\nmetabolic alkalosis\n\nyoung woman, wants to lose weight\ndiuretics or laxative or throws up\n\nlaxatives: prob not diarrhea- bc met alkalosis- so prob not laxatives (and would k to be low in urine- bc lose via GIT and not kidney)\nvomitting: prob not, bc cl hould be low in urine\ndiuretic: met alk, high k in urine, high cl in urine = gittleman, diuretics, (not barter, not mg- bc mg normal (not low)\n\nlook for diuretics in the urine\n\n\n\n\n\n
  73. high ph\n\nmetabolic alkalosis\n\nyoung woman, wants to lose weight\ndiuretics or laxative or throws up\n\nlaxatives: prob not diarrhea- bc met alkalosis- so prob not laxatives (and would k to be low in urine- bc lose via GIT and not kidney)\nvomitting: prob not, bc cl hould be low in urine\ndiuretic: met alk, high k in urine, high cl in urine = gittleman, diuretics, (not barter, not mg- bc mg normal (not low)\n\nlook for diuretics in the urine\n\n\n\n\n\n
  74. high ph\n\nmetabolic alkalosis\n\nyoung woman, wants to lose weight\ndiuretics or laxative or throws up\n\nlaxatives: prob not diarrhea- bc met alkalosis- so prob not laxatives (and would k to be low in urine- bc lose via GIT and not kidney)\nvomitting: prob not, bc cl hould be low in urine\ndiuretic: met alk, high k in urine, high cl in urine = gittleman, diuretics, (not barter, not mg- bc mg normal (not low)\n\nlook for diuretics in the urine\n\n\n\n\n\n
  75. high ph\n\nmetabolic alkalosis\n\nyoung woman, wants to lose weight\ndiuretics or laxative or throws up\n\nlaxatives: prob not diarrhea- bc met alkalosis- so prob not laxatives (and would k to be low in urine- bc lose via GIT and not kidney)\nvomitting: prob not, bc cl hould be low in urine\ndiuretic: met alk, high k in urine, high cl in urine = gittleman, diuretics, (not barter, not mg- bc mg normal (not low)\n\nlook for diuretics in the urine\n\n\n\n\n\n
  76. high ph\n\nmetabolic alkalosis\n\nyoung woman, wants to lose weight\ndiuretics or laxative or throws up\n\nlaxatives: prob not diarrhea- bc met alkalosis- so prob not laxatives (and would k to be low in urine- bc lose via GIT and not kidney)\nvomitting: prob not, bc cl hould be low in urine\ndiuretic: met alk, high k in urine, high cl in urine = gittleman, diuretics, (not barter, not mg- bc mg normal (not low)\n\nlook for diuretics in the urine\n\n\n\n\n\n
  77. \n