L4- Potassium!

Question 1

What does the Na-K-ATPase do? How many ions does it transport?

Answer 1

2K in and 3 Na out

Help determines Ki and Ke which determines neuromuscular excitability - BIG DEAL!!!

Question 2

what are the effects on neuromucsular cells of hypokalemia? hyperkalemia?

Answer 2

Hypokalemia – lowers membrane potential and takes more to reach threshold so cells are less automated - Bradyarrhythmias

Hyperkalemia – Resting membrane potential closer to threshold so easier to fire - more automaticity and random firing can lead to Vtach and VFib

Question 3

WHAT IS THE VALUE OF ECF [K]???? NORMAL RANGE TO KNOW?

Answer 3

3.5- 5 mEq/L

Question 4

What is the short-term mechanism to maintain K+ homeostasis?

What enhances this mechanism? What stops this mechanism?

Answer 4

Transcellular shifts - take it and hide it in cells by activating Na-K-ATPase

Regulated by Beta-adrenergic Agonists or Insulin

Transporter Inhibitors: Alpha-agonists and Beta-blockers

Question 5

What is the long term maintenance mechanism of K+ Homeostasis?

Where in the kidney does this occur?

Answer 5

Long Term Homeostasis maintained by Renal Excretion

1) Glomerulus and PCT: K+ freely filtered and then 50-60% reabsorbed
2) TAL Loop Na-K-2Cl Co-Transporter: K circles and so no real reabs/elimination here but net (+) in lumen allows for paracellular Mg/Ca transport and Loop Diuretics block here so more fluid downstream

**3) CD Principle Cell!!!!!!!! - Majority of K Excretion **

Question 6

How is excretion rate of K in the kidney determined?

Answer 6

Principle Cell K Excretion regulated by:

1) Lumen negative voltage created by reabsorption of Na
2) Fluid flow rate - faster then more excretion
3) ** ALDOSTERONE** - increases, Na-K-ATPase, Increases lumen neg bc more Na in, and Increases number of K+ channels

Question 7

Etiologies for Hypokalemia?

Answer 7

Always have obligate renal loss of K bc can’t make Uk = 0

Therefore if have dietary insufficiency that can cause it (alcoholism, anorexia etc)

GI: Ng suction, vomiting, DIARRHEA

Renal: Hyperaldosteronism, Licorice, RTA, osmotic diuresis, chronic interstitial nephritis , DIURETIC TREATMENT - Furosemide and Hydrochlorothiazide

Question 8

Why does K always drop on loop diuretics? How come you dont die from hypokalemia?

What can be the one risk in diuretics + low salt diet?

Answer 8

Diuretics or Low [Na} cause Increased NA reabsorption in the PCT leading to decreased Distal delivery of NA which limits K Excretion by the Principle cell in the CD

Intravascular volume depletion activates RRAS and increases Na reabsorption and less dleivery to principle cell so less K Excretion

ESTABLISH NEW, LOWER STEADY STATE

Diuretics + Low salt diet for HTN Risk: if you suddenly eat a lot of salt then can get hypokalemiC!!!

Question 9

What are some drug effects on potassium? which ones tend to cause hyperkalemia and which ones cause hypokalemia?

Answer 9

_Drugs that blunt Lumen neg potential = Hyperkalemia: _

• block ENAC channels - Amiloride, Bactrim

Drugs that Increase flow and distal delivery Na = Hypokalemia:

• Diuretics: Furosemide

Drugs that affect Aldosterone = Hyperkalemia

• block Aldo = ACE-inhib, ARBs, Spironolactone

Question 10

How to determine if renal cause of hypokalemia or not?

Answer 10

Uk < 20 - non-renal loss (GI)

Uk > 20 = Renal loss

Question 11

What are the physiological effects of Hypokalemia?

Answer 11

Neuromuscular: Tetany, Ileus, Encephalopathy

Negative Nitrogen Balance

Vasoconstriction

Rhabdomyelisis

Renal: Polyuria and Polydipsia, Loss of concentrating ability, *Alkalosis, Na Retention and Bicarb Retention, Nephropathy

Cardiac: ECG changes and bradyarrhythmia

Question 12

What are the ECK changes seen in Hypokalemia?

Answer 12

Flattened T Wave

new U-wave

Bradyarrhythmias

Question 13

Treatment of hypokalemia?

Answer 13

Fix underlying problem while correcting low K

Oral or IV repletion but w/ IV careful how much you give bc can cause Hyperkalemia!!

Question 14

What is Pseudo-hyperkalemia? What causes it?

Answer 14

Most common cause and not dangerous!!!

Either from:

Mechanical trauma during venipuncture

OR

Increased WBC or PLT - Leukocytosis or thrombocytosis - cells open and break into intravascular space

Common w/ Liquid Tumors

Question 15

What are the etiologies of True Hyperkalemia?

Answer 15

1) Redistribution: Acidemia (increased H+) or Hyperkalemic Periodic Paralysis (rare - high carb meals and transient loss of Na-K-ATPase and bcome paralyzed - weird!?!?)

2) Decreased Excretion - MOst common!

• Kidney disease
• K+ Sparing Diuretics
• Decrased mineralcorticoids - Addison’s
• Hyporeninemic Hypoaldosteronism - Type 4 RTA

3) Increased Inputs

• Endogenous = Hemolysis from Warm Agglutinins OR **Rhabdomyelisis **
• Exogenous - Na substitutes or K+ Penicillin

Question 16

EKG changes in Hyperkalemia?

Answer 16

Peaked T waves

Wide Complex QRS

Loss of P wave

Death!!

MEDICAL EMERGENCY

Question 17

Treatments for Hyperkalemia?

Answer 17

1) STabalize/Antagonize membranes: give Ca2+ to re-establish resting membrane potential + Hypertonic Saline
2) Redistribution of K into cells: Insulin (+ glucose) and Beta-2 Agonists - Albuterol, Sodium bicarbonate?
3) Removal of K+: Diuretics, Potassium Exchange resin to bind it in gut (Na polystyrene), and Dyalysis

Question 18

Diagnostic steps for Hyperkalemia?

Answer 18

Pseudo or True hyperkalemia

• CHECK EKG!!!!!

If it’s true, then you must treat

Question 19

Why do subjects w/ chronic kidney disease tolerate much hgiher K+ levels?

Answer 19

Facilitated acute sequestration of K+ from plasma into cells - they are better at hiding potassium and then less cardiac perturbations

Question 20

Pt w/ Hypokalemia due to increased renal K Secretion (Uk>20) …….Likely causes? Tests?

What is Primary Hyperaldosteronism?

Answer 20

Aldosteronism usualy cause (or iduretics, Renovascular HTN, Renin tumor, Saltwasting disorders, Cushings, Bartter’s)

High plasma Aldo + Low reinin = Primary Hyperaldosteronism

• K depletion occurs when start Thiazide diuretic in HTN tx