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Renal - Rao > Regulation of Potassium Balance > Flashcards

Regulation of Potassium Balance Flashcards

1
Q

Potassium:
• where is it located?
• How is it eliminated?

A

Location:
• INTRACELLULAR Fluid

Elimination:
• Almost completely excreted through the Kidney

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2
Q

Given the storage location and elimination of K, what are 3 important ways its concentration could be increased in the extracellular Fluid or Blood?

A
  1. K can simply be released from ICF storage pool into ECF and blood
  2. Cell Damage can release large amounts of K from the ICF and blood
  3. Impairment of Renal Excretion can also raise levels
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3
Q

What does potassium balance refer to?

• External vs. Internal Balance.

A

K+ levels in the ECF

External:
• Intake throught the Diet and Excretion through GI tract and Kidney

Internal:
• Distribution between intracellular and Extracellular Compartments

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4
Q

In what parts of the kidney is most K reabsorbed in the kidney?
• most important areas for reabsorption?
• Area that becomes significant in Hypokalemia?

A

• PCT, TDLH, TALH, DCT, CCD (basically everywhere except the thin limbs)

2 most important areas of Absorption.
• Proximal Convoluted Tubules
• Thick Ascending LOH

Hypokalemia:
• K collected in the collecting duct becomes important

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5
Q

What Channels are important for potassium transport in the Thick Ascending Loop of Henle?
• describe the co-dependence.

A

APICAL SIDE:
NK2C channel:
• Electroneutral Channel that Brings K+ into the cell

ROMK:
• renal outer medullary potassium channel

NK2C is dependent on ROMK for recycling of some K+ into the TALH lumen

BASOLATERAL SIDE:
NKA:
• Imports K+ into the back side of the celll

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6
Q

Where does Furosemide act?

A

Furosemide:

• works by binding the Cl- channel on NK2C and preventing K+ and Na+ reabsorption

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7
Q

What Channels are important in Principal Cells found in the Cortical and Medullary Collecting tubules (ducts). How do they related to K+ Balance?
• How do they work together?
• hormonal Influence?

A

*ALDOSTERONE - major hormonal influence in the Collecting Tubules (ducts)
Increases expression of the 3 major pumps in the PRINCPAL cells:
Apical: Na+ channel and K+ channel
Basolateral: NKA

How it works:
Basolateral Side: NKA maintains gradient of Low intracellular Na+ and High intracellular K+

Apical:
• Na+ Channel (ENaC)- pumps Na+ INTO principal cells Down its gradient

  • K+ Channel (ROMK)- pumps K+ into LUMEN from principal cells DOWN its gradient
  • Cl- Channel pumps Cl- OUT to interstitium via PARACELLULAR pathway
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8
Q

Where does potassium absorption mostly occur?

• Excretion?

A

Absorption:
• Proximal Convoluted Tubule

Excretion:
• Cortical and Medullary Convoluted Tubules

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9
Q

What are 3 factors that affect K+ secretion in principal cells of the Collecting Tubule (duct)?
• What are these factors dependent on?

A
  1. Serum Potassium Concentration - affects concentration gradient of K across the basolateral membrane
  2. Electrochemical Gradient Across the Luminal Membrane - depends on Na+ concentration
  3. K Permeability of Luminal Membrane - controlled by aldosterone
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10
Q

What would be a consequence on Potassium reabsorption if Na+ was not properly reabsorbed in the Proximal Convoluted Tubule or Loop of Henle?

A
  • More Na will be delivered to the Collecting Duct
  • More Na+ will be Pumped into Principal cells through ENaC => therefore more K+ will be EXCRETED by ROMK

Overall effect = excessive K+ excretion

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11
Q

What affect does excess aldosterone have on K+ metabolism in kidney?
• where is this function seen?

A

Aldosterone - upregulates ENaC, ROMK, and NKA

• Excess aldosterone will lead to an overall INCREASED secretion of K+ so that Na+ can be reabsorbed down its concentration gradient

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12
Q

How does the body adjust K+ uptake and secretion in the collecting duct (tubule) to account for changes in Dietary K+ intake?

A

Ex. HIGH K+ diet:

  1. Increases K concentration gradient
  2. Increased Serum Aldosterone to increase K+ secretion
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13
Q

T or F: Collecting tubule dysfunction of whole kidney dysfunction can lead to HYPERkalemia.

A

True, this is because K+ is no longer excreted in the Collecting Tubule (duct)

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14
Q

What are 3 general factors that will lead to Decreased Renal Postassium Secretion?
• what is the effect on serum levels of potassium with impaired secretion?

A
  1. Renal Failure
  2. Decreased Distal Tubular Flow
  3. Hypoaldosteronism

Impaired secretion will lead to HYPERkalemia

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15
Q

What are two general causes of Increased Renal Potassium Secretion?
• overall effect on serum potassium?

A
  1. INCREASED Na+ DELIVERY to COLLECTING Tubule
  2. INCREASED Aldosterone

**HYPOkalemia will result from these processes

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16
Q

What are some cases in which the amount of Na+ delivered to the Collecting Tubule is increased?

A

Diuretic Use - LOOP diuretics and Thiazide Diruetics that don’t work on ENaC prevent Na+ reabsorption
• by the time the Na+ travels down the ENaC you will have a huge Na+ gradient and K+ will get rapidly shuttled to lumen via ROMK

  • Bartter’s Syndrome
  • Gitelman’s Syndrome
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17
Q

What are some cases in which aldosterone may be increased causing hypokalemia?

A

Secondary:
• Prolonged Vomitting
• Nasogastric Suction

Primary:
• Hyperaldosteronism

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18
Q

What pump is important in maintaining internal balance?

A

NKA - almost all factors that affect internal K balance work through the NKA pump

*note: K+ is constantly exiting through K+ Channels

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19
Q

What are 3 factors that are important in changing K+ concentration inside of Cells?

A
  1. Plasma K concentration
  2. Insulin
  3. Epinephrine
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20
Q

How does insulin work to Change K+ balance?

A

indirectly INCREASES intracellular K+

MOA:
• stimulates NaH exchanger which moves Na+ inside the cells which eases the gradient that NKA must work against

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21
Q

How does Epinephrine work to Change K+ balance?

A

Acts on Beta receptors to INCREASE intracellular K+

MOA:
• Stimulates NKA

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22
Q

What would a Beta Blocker do to Intracellular and Extracellular Potassium?
• albuterol?

A

Beta Blocker:
• Prevents E binding and thus reduces NKA stimulation leading to a REDUCTION in INTRACELLULAR K+

• While less K+ is influxing there is still a good amout EFFLUXING to ECF of the cell so BETA BLOCKER RAISE EXTRACELLULAR K+ concentration

Albuterol:
• Has essentially the same effect as epinephrine

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23
Q

What effect does low serum K+ have on K+ influx and efflux from cells?

A

Low Serum K+ will tend to PULL K+ OUT OF CELLs down its gradient

24
Q

Other Factors that Affect Internal Potassium Balance
• Acid-Base Disturbance
• Plasma Tonicity
• Cell Lysis and Cell Proliferation

A

Other Factors that Affect Internal Potassium Balance
• Acid-Base Disturbance
• Plasma Tonicity
• Cell Lysis and Cell Proliferation

25
Q

What affect do Acid Base disturbances have on K+ levels inside of cells?
• which are more disruptive of the H/K balance; metabolic or respiratory defects?

A

• K+ and H+ shift Reciprocally

ACIDOSIS:
• Metabolic Defects cause more of a disturbance than Respiratory Disturbances
• causes HYPERKALEMIA because H+ is flowing into cells and K+ then flows out

ALKALOSIS:
• leads to HYPOKALEMIA

26
Q

Which will have more of a hyperkalemia associated with it:

• metabolic acidosis due to Mineral Acid or due to Organic Acid

A

Mineral Acids tend to have a greater effect on K+ levels

27
Q

What is the effect of Hypertonicity on K+ levels in the ECF?

A

ECF = Hypertonic
Result is HYPERKALEMIA** (more K+ in the ECF)

  • H2O diffuses out of the cell as a result
  • Some K+ comes with the H2O

Overall:
• Loss of Intracellular H2O increases intracellular K+ concentration

• Increases K+ gradient and some K+ diffuses through the potassium channel

28
Q

What are some common causes of Hypertonicity?

A

• Diabetic Ketoacidosis or Diabetic Hyperosmolar state (caused by inc. Extracellular Glucose concentration)

29
Q

What are some pathogenic causes of cell lysis and cellular proliferation that often cause disruption in K+ balance?

A

Cell Lysis => HYPERkalemia:
• Rhabdomyolysis
• Red Cell Lysis

Cell Proliferation => HYPOkalemia
• Cancer

30
Q

When is a person considered to be Hyperkalemic?

• 3 general causes of hyperkalemia?

A

Serum Potassium greater than 5.5

3 causes:

  1. Excessive Potassium Intake
  2. Decreased Renal Excretion
  3. Internal Redistribution
31
Q

What are some causes of Decreased Renal Excretion of K+?

• common condition that these lead to?

A

All lead to HYPERKALEMIA

  • Acute and Chronic Renal Failure
  • Distal Tubular Dysfunction
  • Decreased Distal Tubular Flow
  • Hypoaldosteronism
32
Q

What are some causes of Defective Potassium Distribution that cause HYPERKALEMIA?

A
  • Insulin Deficiency
  • ß2-adrenergic Blockade
  • Hypertonicity
  • Acidemia
  • Cell Lysis - Rhabdomyolysis
33
Q

What are the EKG manifestations of Hyperkalemia as the disease progresses?

A
  • Tall Peaked T wave (from influx of K1, ATP, and Ach potassium channels)
  • Widened QRS
  • Prolonged PR
  • Loss of P-wave
  • Further QRS widening
  • Ultimately V-tach
34
Q

What are the two reasons that we want to treat hyperkalemia?

A
  • Prevent Cardiac Arrythmias by Stabilization of Cardiac Muscle Cells
  • Lower serum K by moving it either inside cells or outside of the body
35
Q

What treatment do we use to stabilize Cardiac muscle cells in Hyperkalemia?

A

• Intravenous Calcium

36
Q

What are two methods to lowing Serum K+?

• what treatments do we give to achieve this?

A

Moving K+ inside of Cells and OUT of ECF
• Insulin
• ß Agonists
• Bicarbonate

Moving K+ outside of the Body
• Diuretics
• Cation Exchange Resins
• Dialysis

37
Q

What drugs should be given first to someone that comes in hyperkalemic?
• 2nd?
• 3rd?

How long will it take each of these treatments to kick in and how long will they last?

A

1st:
• CALCIUM: Onset 1-3min; Duration 30-60 min

2nd:
• INSULIN: Onset 30 min; Duration 4-6 hours
• BICARB: Onset 15 min; Duration 1-2hrs
• ALBUTEROL: Onset 30 min; Duration 2-4 hrs

3rd:
• FUROSEMIDE: Onset 5 min; Duration 2 hrs
• K-EXCHANGE RESIN: Onset 2-3 hrs; Duration 4-6 hrs

38
Q

What are the 3 general Causes of Hypokalemia?

A
  1. Reduced Potassium Intake (via diet)
  2. Internal Redistribution
  3. Increased Renal or GI Excretion
39
Q

What are some causes of External Potassium loss (aka potassium that’s actually leaving the body, not just moving compartements)?

A
  • Gastrointestinal Losses
  • Cutaneous Losses
  • Renal Losses
40
Q

What are some causes of Internal Redistribution of potassium leading to Hypokalemia?

A
  • Insulin Excess
  • Catecholamine Excess
  • Alkalemia
  • Cell Proliferation
41
Q

What are two causes of NORMOTENSIVE Hypokalemia?

A
  1. Hypokalemia with METABOLIC acidosis

2. Hypokalemia with METABOLIC Alkalosis

42
Q

What are some causes of Hypokalemia with Metabolic Alkalosis?

A
  • Diuretics - LOOP and THIAZIDE
  • Prolonged Vomiting
  • Nasogastric Suction
  • Bartter’s Syndrome
  • Gitelman’s Syndrome
43
Q

What are some causes of Hypokalemia with Metabolic Acidosis?

A
  • Renal Tubular Acidosis (RTA) - Type 1 or 2

* Ureteral Diversion - Into ileum or to Sigmoid

44
Q

Differentiate the causes of Hypokalemia with Metabolic Acidosis on the basis of where the problem arises.

A

Proximal Convoluted Tubule:
• RTA2 (renal tubular acidosis) - K+ and HCO3- can be reabsorbed in PT

Thick Ascending Loop of Henle:
• Furosemide - Block NK2C
• Bartter’s - ineffective NK2C
Extra sodium in carried to CD where it gets exchanged for K+ (via ENaC and SOMK)

Distal Tubule:
• Thiazide Diuretics - blockage of Na-Cl transporter
• Gitleman’s Syndrome - Blockage of Na-CL transporter
Extra sodium in carried to CD where it gets exchanged for K+ (via ENaC and SOMK)

Collecting Duct Dysfunction:
• RTA type 1 hypokalemia

45
Q

What are the 3 outcomes that result from excess H+ and Cl- loss from vomitting?
• how do they come about?

A

Elevated Serum Aldosterone:
• causes increase Na+ reabsorption
***Result: Increases Electronegativity of Lumen

Loss of Cl- from HCl in vomit:
• Less Cl- delivered to distal tubule
• MORE non-absorbable HCO3- to distal tubule (because it can’t be absorbed in the LOH like Cl)
***Result: Increased Electronegativity of Lumen

Elevated Levels of HCO3- in BLOOD:
• due to loss of H+ (LeChatelier’s pushes equn. to the right)

ELECTRONEGATIVITY in Tubular Lumen causes:
• Increased SECRETION of K+ and H+

3 ULTIMATE OUTCOMES:
• Hypokalemia
• Metabolic Alkalosis
• PARADOXICAL Aciduria

46
Q

What are some causes of HYPERTENSIVE hypokalemia?

A

Diseases are caused by TOO MUCH ALDOSTERONE - either directly or through too much renin

Hyperreninemia:
• Renal Artery Stenosis
• Renin-Secreting Tumor

Primary Hyperaldosteronism (Conn’s Syndrome):
• Adrenal Hyperplasia
• Adrenal Tumor

*OR can be caused by too much Glucocorticoid that can weakly bind aldosterone receptor

Cushing’s Syndrome
• Exogenous, Adrenal, Pituitary

Congenital Adrenal Hyperplasia
• Enzymatic Defects in Cortisol Biosynthesis

47
Q

What is the most common cause of excess glucocorticoid that caueses Hypokalemia with Hypertension?
• why are Hypokalemia and HTN seen?

A

EXOGENOUSLY induced CUSHING’s Syndrome
• ppl. w/ transplants, COPD, Autoimmune disease etc. that require long term steriod

Hypokalemia:
• Caused by increased Na+ absorption (via more ENaC, ROMK, NKA production)

• Na+ is indirectly exchanged for K in the lumen as it travels down its gradient

Hypertension:
• Na+ retention increases Blood Volume

48
Q

What EKG changes are associated with Hypokalemia?

A
  • Flat - T wave
  • Prominent- U wave
  • Depressed - ST Segment

**U-wave is Pathopneumonic for Hypokalemia

49
Q

Contrast the Arrhythmia created by hyperkalemia and hypokalemia.

A

Hyperkalemia:
• BRADYARRYTHMIA

Hypokalemia:
• TACHYARRYTHMIA

50
Q

T or F: severe symptoms are often associated with chronic hypokalemia.

A

FALSE, chronic hypokalemia is usually asymptomatic

51
Q 
What symptoms are seen in the following systems when someone gets hypokalemic? 
• Cardiac
• Smooth Muscle
• Skeletal Muscle
• Renal
A

Cardiac:
• EKG changes
• (tachy) Arrhythmias

Smooth Muscle:
• Hypertension
• Intestinal ileus

Skeletal Muscle:
• Weakness
• Rhabdomyolysis

Renal:
• Nephrogenic Diabetes Insipidus

52
Q

What are two general treatments administered for hypokalemia?

A
  1. Potassium Replacement

2. Potassium Sparing Diuretics

53
Q

Why determining someone’s potassium deficit so difficult?

A

We can only measure Serum Potassium as an estimate of INTRACELLULAR potassium, which is where the actual deficiency is.

54
Q

What is the problem with rapid infusion of potassium for someone with Potassium Deficiency?

A

Rapid K+ infusion can cause Cardiac Arrest

55
Q

What specific compound would you give someone who was Hypokalemic?
• how would you do this?

A

KCl or KPO4 can be given ONLY if there is an accompanying phosphate deficiency

SLOW IV infusion over a period of 2 hours

You can also give ORAL KCl

56
Q

What is the typical treatment for CHRONIC hypokalemia?

A

POTASSIUM SPARING DIURETICS:
Aldosterone Receptor Blockers/Mineralcorticoid antagonists
• Spironolactone
• Eplernone

ENaC sodium Channel Inhibitors
• Amioride
• Triamterene

These work because they act on the source in the Collecting tubule that typically creates the hypokalemia

Renal - Rao (13 decks)

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