Disorders of K+ Metabolism (Linus) Flashcards
What are two important hormonal/chemical mediators of K+ balance in the body?
Insulin and catecholamines
(K+ is a stimulus for insulin secretion. The two are closely correlated. From a pathophysiologic perspective B2 receptors [non B1] can move K+ from the ECF to the ICF so nonselective BBlockers prevent K movement (propanolol), while selective BB (metoprolol) do not)
For most clinical purposes, the K+ in the DCT can be considered as 0. (Actually 10-15% but doesn’t matter). The most important site for clinically relevant K+ movement is in the cortical collecting tubule and medullary tubule.
nuff said.
What are the three main categories of hypokalemia?
1) Chronic - Decreased Body K (Decreased intake or increased losses [GI or Renal])
2) Acute - Trancellular shift (stress eg. catecholamine excess [medications], physiologic stress [chest pain, asthma, drug withdrawal], or insulin excess [rare])
3) Spurious (lab artifact)
What differentiates renal K+ losses from extrarenal losses?
Urine K levels.
20-40 is considered renal (kidneys failing to retain K even when body K is low)
Given an extrarenal loss of K, what might be the two big categories you would consider in a patient history?
Metabolic acidosis (eg diarrhea) Decreased dietary intake
Given a renal cause of hypokalemia, what three categories might you consider asking about in a patient history?
Metabolic Alkalosis
Normal pH
Metabolic Acidosis (eg DKA)
What are the progressive EKG changes at increasing K+ levels?
No change, peaked T waves, Widened QRS with flattened P wave, Sine wave (if sine wave, patient will arrest promptly. Medical emergency)
What is the first thing you should do when seeing a hyperkalemic patient?
Order an EKG.
What are the three broad categories of hyperkalemia?
1) Chronic (Increased Total Body K)
2) Acute (Transcellular Shift)
3) Spurious (lab artifact)
What are some causes of acute hyperkalemia?
1) Inadequate insulin response - diabetes
2) Medications - nonselective BB might impede response to big oral K+ intake
3) Ischemic body part (PAD, Rhabdo, MI, dead limb, etc)
What are some causes of chronic hyperkalemia?
1) DIETARY INTAKE is almost never the cause. UNless yo kidneys don’t work
2) GFR isn’t the problem.
The problem is K secretion by the CCT, and you will see low urinary K. The major determinant is aldosterone. With too much aldo, receptor is activated and you get high urine k and low serum k. If you have too little aldo, you will get high serum K, low urine K. (Check the aldo level, then figure out whether you have a production problem or a response problem to the aldosterone)
What is Tx for hyperkalemic patient with EKG changes?
Calcium gluconate immediately, then sodium bicarb, glucose, insulin and albuterol (all move from the ECF to the ICF), then dialyze the patient.
Case 1: 54 y/o man with acute MI. Cardiac arrest in ER, 145/2.8 (k)/120/15 ECG Vfib. Cause?
Hypokalemia. Tx is defibrillate, IV potassium, say a prayer that the K comes in fast enough. Difficult to give large loads of K
24 y/o with aids. Diarrhea for days, K of 2.6. Urine k
GI problem, acidotic with diarrhea, give K. Treat diarrhea
(Acidosis/alkalosis) ______ increases potassium secretion, hence tends to produce hypokalemia.
Alkalosis
But how does aldosterone increase K+ secretion?
First, recall that aldosterone increase the number of Na/K/ATPase pumps on the basolateral surface. Obviously this increases the rate of potassium entry (enhanced step 1) and the intracellular concentration of K+ (enhanced step 2), as was seen in the mass action effect. Secondly, recall that aldosterone also increases the number of apical sodium channels. This will increase the rate of apical potassium secretion (step 2) because it enhances the passive counter flow of sodium inward across the apical membrane in exchange for outward potassium movement. Thirdly, aldosterone also increases the number of apical potassium channels, making it easier for potassium to flow into the lumen in step 2. The net effect is a strong enhancement of potassium secretion by aldosterone
Fast flow through the tubules will increase/decrease K+ excretion?
Increase. Because the solution moves so fast, a favorable osmotic gradient for the excretion of K+ is maintained.
Name the loop diuretics. How do these waste potassium when they inhibit the Na/Cl/Cl/K cotransporter?
Recall that the Na/K/2Cl co-transporter, through its transport of NaCl makes the interstitium hypertonic, thus creating an osmotic gradient for water reabsorption in both the descending limb and in the fine tuning segments. Thus inhibition of this process will diminish the osmotic gradient for the reabsorption of water, hence more water will remain in the tubule. Thus an increased flow of tubular fluid enters the fine-tuning segments due to the inhibition of descending limb water. Further, this increased flow will self-augment everywhere water is reabsorbed in the fine tuning segments themselves. In this way loop diuretics cause a large increase in tubular flow at the point of potassium secretion, greatly enhancing it.
State the effect on SERUM K: Insulin
Decrease
State the effect on SERUM K: Beta Blockers
Increase
State the effect on SERUM K: Alkalosis
Decrease
State the effect on SERUM K: Digoxin
Increase
State the effect on SERUM K: Hyperaldosteronism
Decrease
State the effect on SERUM K: Furosemide
Decrease
