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Pathophysiology - Urinary Tract > Disorders of Potassium Metabolism > Flashcards

Disorders of Potassium Metabolism Flashcards

1
Q

Where is most of our potassium stored in the body, and how do we process it each day?

A

98% is stored intracellularly, mostly intramuscularly. ECF has very low levels.

Each day we intake about 100 mEq and excrete 90% renally and 10% through the stool.

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2
Q

How does processing of potassium happen acutely around mealtime or during advanced renal failure?

A

Mealtime - potassium load is shifted to liver and muscle cells to temporarily buffer the spike in blood potassium which may be dangerous

Advanced renal failure - excretion of potassium in stool can be as high as 40%

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3
Q

What ratio determines the resting membrane potential of cells and why does this matter?

A

Proportional to negative (Intracellular K+ concentration / extracellular K+ concentration)

Because K+ is roughly 100x more permeable than sodium

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4
Q

What matters more: changing intracellular potassium or extracellular and why? How does it change?

A

Changing extracellular -> will be a greater % of total change and change the ratio for electrical potential

A slight increase in extracellular K+ would destroy the electrical gradient and lead to cell hypopolarization -> must be tightly regulated

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5
Q

What factors stimulate the Na+/K+-ATPase to maintain the gradient?

A

Catecholamines
Insulin
Hyperkalemia

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6
Q

What effect to catecholamines have on potassium homeostasis via the Beta-2 receptors? What would propranolol do?

A

B2 receptors promote entry of potassium into primarily skeletal muscle and liver cells -> activate Na/K ATPase

Propanolol would block this B2 receptor effect and may contribute to hyperkalemia

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7
Q

What effect do alpha agonists have on potassium homeostasis and how?

A

Impair entry of K+ into cells ->increase serum K+

Alpha2 receptors also block insulin release
-> decreased insulin leads to a rise in K+ levels

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8
Q

How does insulin affect K+?

A

Insulin promotes entry of K+ into skeletal muscle directly by increasing the number of Na/K ATPases

Insulin stimulates Na/H exchanger in liver, bringing Na+ into the cell. Every 3 turns of this leads to 2 K+ brought into the liver cell via the Na/K ATPase

Insulin allows K+ entry into cells passively.

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9
Q

How does exercise affect serum potassium levels and why?

A

Increases serum potassium levels directly proportionately to the severity of exercise

  • > K+ release is the stimulus for vasodilation and increased blood flow
  • > ATP-gated K+ channels begin to run as ATP is depleted
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10
Q

What effect does metabolic acidosis have on potassium homeostasis and why?

A

Causes hyperkalemia

  • > decreased ability to run Na/H antiporter since ECF is already acidic
  • > less Na+ inside the cell to run Na/K ATPase -> potassium stays outside of the cells
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11
Q

Is the hyperkalemic effect of metabolic acidosis worse with mineral or organic acids?

A

Worse with mineral acids, since the anions can’t enter the cell and must stay in the blood

Organic acids can be transported into the cell so the effect of hyperkalemia will be less dramatic

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12
Q

What will be the effect of respiratory acidosis, respiratory alkalosis, and metabolic alkalosis on K+ levels?

A

Respiratory acidosis - hyperkalemia, like all acidosis

Respiratory / metabolic alkalosis - hypokalemia (Na/H exchanger can work faster)

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13
Q

What effect will hyperosmolarity have on blood potassium levels and why?

A

Hyperosmolarity - increased K+ levels

  • > Osmotic drag = K+ leaves the cells with water
  • > Decreased water inside cells also concentrates K+, passive movement out of cells
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14
Q

How can growth / lysis of cells affect K+ balance?

A

Lysis syndromes (rhabdo, hemolysis, or tumor lysis) - hyperkalemia

Rapid growth - hypokalemia, especially in initial response of megaloblastic anemia to B9/B12 therapy

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15
Q

How is the majority of the potassium reabsorbed in the kidney?

A

Majority in proximal tubule

Early proximal tubule - due to solvent drag, from movement of water and sodium into cells, concentrating K+

Late proximal tubule - due to paracellular diffusion, as lumenal potential becomes positive

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16
Q

What is potassium’s major role in the thick ascending loop of Henle and how does it accomplish this?

A

Rapidly cycles through NKCC then out into the tubule against via ROMK in order to facilitate rapid NKCC movement for reabsorption of sodium

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17
Q

How does the distal convoluted tubule and collecting duct prevent potassium wasting under physiologic conditions?

A

With low K+ loads, principle cells in DCT downregulate ROMK

Furthermore, alpha-intercalated cells in the collecting duct upregulate the H+/K+ ATPase antiporter if K+ is low.

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18
Q

How does increasing the activity of ENaC relatively affect ROMK via principle cells?

A

Increased ENaC activity -> more negative intraluminal potential as Cl- or non-reabsorbable anions (i.e. penicillin) will stay in lumen longer or forever, respectively

Negative potential increases ROMK activity and hence K+ wasting

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19
Q

What are the three primary actions of aldosterone which increase K+ secretion overall?

A
  1. Increased number of ENaC in principle cells
  2. Enhanced Na/K ATPase activities in basolateral membrane
  3. Increased ROMK luminal membrane
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20
Q

What is the general underlying problem of the aldosterone paradox?

A

High K+ levels stimulate aldosterone secretion, which preferentially leads to K+ excretion within minimal Na+ reabsorption

Angiotensin II also stimulates aldosterone secretion, which preferentially leads to Na+ reabsorption with minimal K+ excretion

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21
Q

What justifies the aldosterone paradox?

A

Angiotensin II - stimulates the WNK kinases and reabsorbs more Na+ via the NCC in the early DCT so less sodium load is delivered to late DCT / principle cells, preventing K+ losses

K+ stimulation of aldosterone - WNK kinases not affected, to K+ is lost more readily, and same amount of Na+ is reabsorbed

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22
Q

What is the function of the WNK kinases? What else are they stimulated by other than Angiotensin II?

A

They lead to removal of ROMK channels in the distal nephron -> Also stimulated by low blood potassium levels

-> make sense because we want to save potassium from excretion

23
Q

What effect does distal flow rate have on K+?

A

Increased flowrate = less K+ already sitting in lumen destroying gradient = more K+ losses

24
Q

What effect does pH have on K+ reabsorption and why?

A

Acidemia - increases K+ reabsorption, can quickly run H/K antiporter -> acidemia is associated with hyperkalemia

Alkalemia - decreases K+ reabsorption, cannot run H/K antiporter -> alkalosis is associated with hypokalemia

25
Q

What potassium change do each of the following events predispose to and why?

Myocardial infarct, alcohol withdrawal, asthma attack, thyrotoxicosis

A

Increased stress with increased catecholamines = beta2 stimulation = hypokalemia

26
Q

What are extrarenal mechanisms of K+ loss?

A
  1. Diarrhea / vomiting - direct loss of K+ from GI system, but renal mechanisms may contribute. Especially LAXATIVE use.
  2. Increased sweat loss - marathon runners or cystic fibrosis
27
Q

What are the renal mechanisms of hypokalemia?

A
  1. Diuretics - non-K+-sparing
  2. Mineralocorticoid excess
  3. Increased flow of Na+ and water to collecting tubules - salt-loading and osmotic diuretics
  4. Sodium reabsorption with a non-reabsorbable anion
28
Q

What are the non-reabsorbable anions which can be reabsorbed with sodium?

A

HCO3-, sulfate, penicillin, ketones

29
Q

What muscle problems can be induced by hypokalemia?

A

Muscle weakness / cramps / rhabdomylosis, can lead to paralytic ileus

-> decreased K+ to be released leads to inadequate blood flow

30
Q

What ECG changes are characteristic of hypokalemia?

A

U waves and flattened T waves

due to increased negativity of resting potential and slow repolarization

Can cause arrhythmia

(just remember that peaked T waves are hyperkalemia due to rapid repolarization and ur gucci)

31
Q

What endocrine abnormalities are induced by hypokalemia?

A

Decreased insulin secretion (already too much K+ in cells)

Increased renin with decreased aldosterone (aldosterone paradox)

32
Q

What renal pathologies does hypokalemia induce?

A

Impaired renal concentrating ability, increased ammonia production (worsens alkalosis), vacuolization of proximal tubular cells, interstitial nephritis (scarring)

Predisposition towards kidney stones from hypocitraturia

33
Q

How is extrarenal vs renal loss of K+ identified?

A

Extra-renal loss = K+ is conserved in urine, will be less than 25 mEq loss per day

Renal loss = K+ increased in urine despite hypokalemia = >25 mEq loss per day

34
Q

What are the causes of renal K+ loss with hypertension and mineralocorticoid excess? Which is most common?

A
  1. Hyperaldosteronism, deoxycortisone, and ACTH producing tumors.
  2. Renin-secreting tumors
  3. Renal Artery stenosis - most common
35
Q

What are the causes of renal K+ loss with hypertension and no mineralocorticoid excess? These conditions mimic HTN with mineralocorticoid excess.

A
  1. Liddle’s syndrome

2. Licorice ingestion -> syndrome of apparent mineralocorticoid excess

36
Q

What is syndrome of apparent mineralcorticoid excess and how does it work?

A

Either a hereditary deficiency in 11B-hydroxysteroid DH or inhibitor of enzyme (glycyrrhetinic acid in licorice) which is needed to convert cortisol to inactive cortisone in principal cells

37
Q

What is Liddle’s syndrome? How is it inherited?

A

Gain of function mutation -> constitutively open ENaC channels in principal cells
-> leads to hypertension without mineralocorticoid excess

Since it’s gain of function it’s autosomal dominant

38
Q

How do you remember Bartter syndrome vs Gitelman syndrome vs Liddle syndrome?

A

They are in alphabetical order based on place of defect

Bartter - TALH
Gitelman - DCT
Liddle Syndrome - Collecting duct

39
Q

What are the causes of renal K+ loss without HTN?

A 
Vomiting
Diuretics - increased Na+ load
Bartter syndrome
Gitelmans syndrome
Renal tubular acidoses types I and II
40
Q

Why does vomiting cause hypokalemia?

A

Vomiting - causes alkalosis, so less K+ can be reabsorbed in collecting duct

41
Q

What is Bartter syndrome?

A

Defect in TALH -> defective NKCC transporter

42
Q

What is Gitelmans syndrome?

A

Defective DCT -> defective NCC (Na/Cl cotransporter)

43
Q

What is pseudohyperkalemia?

A
  1. High K+ due to difficulty with venipuncture which causes local mechanical trauma and muscle K+ release.
  2. Serum H+ is always higher K+ than plasma K+ when measured in the lab because of clotting process leads to lysis. High WBC / platelet counts can make this effect greater
44
Q

What are some exogenous and endogenous sources of increased K+ load?

A
  1. Exogenous - food, salt substitute, and some drugs

2. Endogenous - hemolysis, rhabdomyolysis, tumor lysis

45
Q

What two drug can cause an intracellular to extracellular K+ shift?

A

Digitalis overdose - inhibits Na/K ATPase

Succinylcholine - depolarizing blockade favors K+ exit

46
Q

In what conditions will inadequate urinary excretion lead to hyperkalemia?

A
  1. Very late stage renal failure - GFR <20
  2. Effective circulatory volume depletion - K+ excretion limited by small urine volume
  3. Hypoaldoesteronism
47
Q

What antibiotic causes a Type IV renal tubular acidosis and what is the mechanism?

A

Trimethoprim - blocks ENaC
-> hyperkalemia

Note that RTA4 is associated with hyperkalemia

48
Q

What is meant by renal adaptation to potassium loading?

A

Increased serum K+ and aldosterone levels enhance Na/K ATPase levels. Overtime this change no longer requires high levels of aldosterone, and the kidney can excrete K+ even at very low GFRs

49
Q

What are the clinical ECG manifestations of hyperkalemia? Are these more serious than hypokalemia?

A

Wide QRS with peaked T waves -> arrhythmias

QT intervals are shortened -> rapid repolarization

-> can cause bradycardia

Widened QRS with severe hyperkalemia can lead to loss of P waves and eventual Vfib

More serious than hypokalemia, more likely to cause emergent arrhythmia

50
Q

What are the clinical muscle and endocrine manifestations of hyperkalemia?

A

Muscle weakness and paralysis

Endocrine - increased aldosterone and increased insulin secretion, while decreasing renin

51
Q

What is indicative of a renal defect leading to hyperkalemia?

A

Urine potassium of less than 25 mEq

Well adapted kidneys can excrete 200 mEq K per gram creatinine

52
Q

What drugs are used in the rapid treatment of hyperkalemia?

A

Calcium gluconate - stabilizes membrane of cardiomyocytes to prevent over-excitability
Insulin and glucose - increased K+ entry into cells

53
Q

What other drugs are used in the early treatment of hyperkalemia (not within first 10 min)

A

Sodium bicarbonate - if acidemic -> increase K+ excretion

Albuterol - increased K+ entry into cells via Beta-2 agonism

Kayexalate - removal of excess K+ from body, delayed onset

Dialysis

Pathophysiology - Urinary Tract (14 decks)

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