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Renal by Minnie > SM 193a - Potasisum > Flashcards

SM 193a - Potasisum Flashcards

1
Q

Why is insulin an effective treatment for hyperkalemia?

A

Insulin increases Na+ entry into the cell

  • -> Increased activity of the Na+/K+ ATPase
    • Pumps Na+ out of the cell and K+ in
  • -> Removal of K+ from the serum

Note: you need to also give glucose when you give insulin for hyperkalemia to prevent hypoglycemia!

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2
Q

How can electrolyte levels help you determine whether a patient has Barter’s syndrome, or bulimia?

A

Urine analysis: Cl- is the key

  • Barrter’s syndrome
    • High Na+, K+ and Cl- in the urine
      • The Na+/K+/2Cl- cotransporter is blocked, so none of these are reabsorbed
  • Bulemia (vomiting)
    • Variable Na+
    • High K+
    • Low Cl-
      • Alkyosis is responsive to saline
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3
Q

What is the normal range of plasma K+?

A

3.5-4.9 mM

<3.5 mM = hypokalemia

>4.9 mM = hyperkalemia

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4
Q

How does volume depletion or expansion affect K+ secretion?

A

No effect

  • Decreased ECF volume -> decreased distal delivery of Na+ -> increased aldosterone, but no change in K+
  • Increased ECF volume -> increased distal delivery of Na+ -> decreased aldosterone, but no change in K+

**(Not super clear on this, since aldosterone definitely affects K+ homeostasis…)**

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5
Q

How does digitalis toxicity affect K+ homestasis?

A

Digitalis toxicity (due to digoxin) -> hyperkalemia

Digoxin blocks the Na+/K+ ATPase

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6
Q

If a patient has low cortisol and high plasma renin activity, what kind of aldsoterone deficiency do they have?

A

Aldosterone + Glucocorticoid deficiency

Ex: Addison’s disease

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7
Q

If you consume 100 mEq of K+/day, how much will be excreted in the urine?

What happens to the rest?

A

90-95 mEq excreted in the urine (through the kidneys)

5-10% mEq excreted in the feces

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8
Q

What is the etiology of non-depletional hypokalemia?

A

Transcellular redistribution: K+ is transferred from ECF to ICF

Body K+ is normal, but plasma K+ is low

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9
Q

What are the most common causes of depletional hypokalemia?

A
  • Extrarenal losses
    • GI tract losses
      • Vomiting, diarrhea, intestinal fistula, tube drainage
  • Renal losses
    • Mineralcorticoid excess
    • Diuretics
    • Bartter syndrome
    • Gitelman syndrome
    • Renal tubular acidosis
  • Low intake
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10
Q

How does decreased plasma osmolality affect K+ homeostasis?

A

Decreased osmolality -> decreased plasma K+

Decreased plasma osmolality shifts water into the cell, dragging K+ along with it

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11
Q

Which drugs block Na+ channels in the cortical collecting duct

A
  • Amiloride*
  • Triameterene*
  • Trimethoprim
  • Pentamidine

*K+ sparing diuretics

Spironolactone and eplerenone are also K+-sparing diuretics, but they act by blocking the aldosterone receptor, rather than blocking the Na+ channel

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12
Q

What is the first EKG manifestation of hyperkalemia?

A

High T wave

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13
Q

Where in the kidney tubule is the heavily-regulated K+ secretion and reabsorption pathway?

A

Cortical collecting duct

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14
Q

What stimulus drives K+ secretion through Maxi-K?

A

Increased flow in the lumen creates a chemical gradient

  • Flow removes K+ in the lumen
  • K+ flows down its concentration gradient through Maxi-K
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15
Q

What protein maintains the difference of intracellular and extracellular K+ concentration?

A

Na+/K+ ATPase

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16
Q

What causes of hypokalemia are associated with metabolic alkalosis?

A
  • Vomiting
  • Diuretics
    • Thiazide and loop
  • Bartter’s syndrome
  • Gitelman’s syndrome
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17
Q

What is the main difference in Na+ reabsorption between the early and late distal convoluted tubule?

A
  • Early: Na+/Cl- Cotransporter
    • Electrically neutral
  • Later: ENaC and ROMK
    • ​Electric neutrality depends on K+ secretion paired ot Na+ reabsorption
    • This is the same set-up that principal cells in the cortical collecting duct have
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18
Q

Which cells in the kidney tubule are most important for K+ secretion?

A

Cortical collecting duct principal cells

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19
Q

What are the common etiologies of hypokalemia associated with normal or low blood pressure?

A
  • Diuretics
    • Thiazides and loop diuretics
    • These might be prescribed for HTN, but over-use -> hypovolemia -> hypotension
  • Proximal & distal tubular acidosis
  • Bartter’s syndrome
  • Gitelman’s syndrome
  • Drug-induced
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20
Q

Which cells have the highest intracellular K+ concentration?

A
  • Skeletal muscle
  • Liver
  • Erythrocytes
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21
Q

Would inhibition of the Na+/K+ ATPase result in hyperkalemia or hypokalemia?

A

Hyperkalemia

If the Na+/K+ ATPase cannot pump K+ in to the cell, more will remian in the serum, resulting in hyperkalemia

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22
Q

What cause of hypokalemia are associated with metabolic acidosis?

A

Diarrhea (Low serum K+, low urine K+

Renal tubular acidosis (Low serum K+, High urine K+)

23
Q

What are the renal causes of hyperkalemia?

A
  • Decreased GFR
  • Aldosterone deficiency
  • Decreased distal Na+ delivery
  • Blockade of Na+ channels in the cortical collecting tubule
    • Amiloride
    • Spironolactone
24
Q

Which hormones upregulate activity of the Na+/K+ ATPase?

A
  • Insulin
    • -> Na+ entry into the cell
    • -> stimulation of the Na+/K+ ATPase
  • Epinephrine (Beta-2 agonist)
    • -> Formation of cAMP
    • -> Stimulation of Na+/K+ ATPase
    • Also causes a minor release of K+ into cells via alpha-1 stimulation
25
Q

Describe the mechanism for K+ reabsorption in the proximal tubule

A

Paracellular pathway

H2O is reabsorbed and K+ comes with ti

This reabsorbs about 67% of filtered K+

26
Q

What are the common causes of iatrogenic renal hyperkalemia?

A
  • ACE inhibitors (-prils)*
  • ARBs (-sartans)*
  • Spironolactone
  • Chronic heparin therapy
  • Cyclosporin A
  • NSAIDs

These drugs are contraindicated in patients with kidney disease

*these drugs inhibit the RAAs, leading to low aldosterone -> decreased Na+ reabsorption -> decreased K+ secretion

27
Q

What are the EKG effects of hypokalemia?

A

As hypokalemia worsens, the following EKG changes appear:

  • Low T wave
  • High U wave
  • Low ST segment
28
Q

What stimulus drives K+ secretion through ROMK?

A

Electric gradient

  • Na+ reabsorption through ENaC creates negative charge in the lumen and positive charge in the cortical collecting duct principal cell
  • K+ is secreted through ROMK to balance the charges
29
Q

How can you tell whether a patient has Bartter’s syndrome or is taking secret loop diuretics?

A
  • Bartter’s and Gitelman’s -> low magnesium (But not conclusive)
  • Genetic analysis
30
Q

How does metabolic acidosis affect K+ homeostasis?

A

Metabolic acidosis increases plasma K+

Acidosis ->

  • Inhibition of the Na+/K+ ATPase
  • Activation of the ATP-sensitive K+ channels
31
Q

How does exercise affect K+ homeostasis?

A

Exercise causes the release of K+ from skeletal muscle cells, resulting in increased plasma K+

32
Q

What is the effect of hypokalemia on the heart?

A

Hypokalemia hyperpolarizes the myocyte (more negative membrane potential)

It is less likely to fire an action potential

33
Q

Why might plasma K only be slightly reduced even with substantial body K+ depletion?

A

K+ is an intracellular ion

We can lose a lot of K+ from body without major changes in plasma K+ if it is moved from the cells to the plasma

34
Q

The intracellular concentration of K+ is ______ mEq/L

The extracellular concentration of K+ is ______ mEq/L

A

The intracellular concentration of K+ is 150 mEq/L

The extracellular concentration of K+ is 4 mEq/L

35
Q

Which proteins in the principal cells of the cortical collecting duct are responsible for the secretion of K+?

A
  • ENaC
    • Na+ into cell, creates negative charge in the lumen
  • ROMK
    • ​Secretes K+ into the lumen in response to negative charge in the lumen created by Na+ reabsorption (electrical gradient)
  • Maxi-K+
    • ​Secretes K+ in response to increased flow in the lumen (chemical gradient)
      • Increased flow removes the K+ secreted into the lumen, maintaining the concentration gradien

**The Na+ channel is more important than the K+ channel in the regulation of K+ secretion!**

36
Q

What diseases might produce hypokalemia associated with hypertension?

A
  • Primary hyperaldosteronism
  • Cushings syndrome
37
Q

What is the first EKG manifestation of hypokalemia?

A

Low T wave

38
Q

What is the difference between depletional hypokalemia and nondepletional hypokalemia?

A
  • Depletional
    • Low body K+ - there is no extra K+ in cells
    • Due to extra renal losses, renal losses, or low intake
  • Nondepletional
    • Body K+ is normal
    • Due to transcellular redistribution
39
Q

How does metabolic alkylosis affect K+ homeostasis?

A

Metabolic alkylosis decreases plasma K+

  • Activation of the Na+/K+ ATPase
  • Inhibition of the ATP-sensitive K+ channels
40
Q

How does aldosterone affect K+ homeostasis?

A

Aldosterone decreases serum K+

  • Aldosterone increases the activity of the Na+/K+ ATPase
    • More K+ pumped out of the plasma and into the cell
  • Aldosterone increased the activity of ENaC (collecting duct)
    • Increased Na+ reabsorption -> Increased K+ secretion

Aldosterone acts mostly on the DCT and collecting duct

41
Q

What is the effect of hyperkalemia on the heart?

A

Hyperkalemia depolarizes the myocyte (membrane potential becomes less negative)

This makes the cell more excitable, and more likely to fire an action potential

42
Q

What causes Gitelman’s syndrome?

What is the effect on K+ homeostasis?

A

LOF mutation in the Na+/Cl- cotransporter in the distal tubule leads to hypokalemia (but less severe than Bartter’s)

  • K+ and Na+ stays in the lumen (not reabsorbed)-> Increased Na+ delivery to the cortical collecting duct
    • -> Increased Na+ reabsorption through ENaC
    • -> Increased K+ secretion through ROMK
    • -> Hypokalemia
  • Na+ wasting
    • -> Increased aldosterone
    • -> Further promotes Na+ reabsortion through ENaC
    • -> Further increases K+ secretion through ROMK
43
Q

What causes Bartter’s syndrome?

How does it affect K+ homeostasis?

A

Defect the K+/Na+/2Cl co-transporter in the thick ascending limb that leads to hypokalemia

  • K+ and Na+ stays in the lumen (not reabsorbed)
    • -> Increased Na+ delivery to the cortical collecting duct
      • -> Increased Na+ reabsorption through ENaC
      • -> Increased K+ secretion through ROMK
      • -> Hypokalemia
  • Na+ wasting
    • -> Increased aldosterone
    • -> Further promotes Na+ reabsortion through ENaC
    • -> Further increases K+ secretion through ROMK
  • Also causes volume depletion due to wasting of Na+ and Cl-
44
Q

How does increased plasma osmolality affect K+ homeostasis?

A

Increased osmolality -> Increased plasma K+

Increased plasma osmolality shifts water out of the cell, dragging K+ along with it

45
Q

What are the major causes of hypokalemia due to abnormal transcellular distribution of potassium?

(Non-depletional hypokalemia)

A
  • Excess insulin
  • Beta-adrenergic agonists (albuterol)
  • Acute illness
  • Alkalemia

All stimulate the Na+/K+ ATPase

46
Q

Why would you suggest that Type I diabetics eat a low-potassium diet?

A

K+ storage in the tissues protects the body from high K+ concentration if you eat more than ~100 mEq/day of K+

However, this mechanism depends on insulin to stimulation the Na+/K+ ATPase

Without insulin, you cannot shovel K+ into the tissues, and plasma K+ will remain high (which can be bad)

47
Q

What happens to your plasma K+ concentration if you consume too much potassium in your diet?

A

It will remain the same

You can excrete ~ 100 mEq/day of K+ in the urine and feces. If you consume more than this, insulin and epinephrine stimulate K+ uptake into the cells; plasma [K+] remains normal

  • The cells/tissues can store up to 3445 mEq of K+ - they are a protective mechanism; this is very important for people with renal failure
  • The kidney can also adapt to reabsorb or secrete more K+ depending on depletion/excess (if they are working properly)
48
Q

What are the most dangerous effects of inhibition of the Na+/K+ ATPase?

A

Hyperkalemia -> Death

49
Q

Why might it be dangerous to give an ACE inhibitor to a patient with renal failure?

A

ACE inhibitor ->

  • -> Decreased Angiotensin II
  • -> Decreased aldosterone secretion
  • -> Decreased Na+ reabsorption (in the cortical collecting duct)
  • -> Decreased K+ secretion (in the cortical collecting duct)
  • -> Potential hyperkalemia

Patients with healthy kidneys are usually okay, but this can be dangerous for patients in renal failure

50
Q

How do beta-blockers affect K+ homestasis?

A

Beta blockers can cause hyperkalemia

Inhibition of the Na+/K+ ATPase

51
Q

Why does aldosterone deficiency result in hyperkalemia?

A
  • No aldosterone
  • -> cannot increase Na+ reabsorption
  • -> K+ secretion does not increase
  • -> Hyperkalemia
52
Q

Decribe the mechanism for K+ reabsorption in the thick ascending limb of the Loop of Henle

A
  • Apical
    • K+/Na+/2Cl- cotransporter
      • More active than the ROMK K+ channel for secretion
  • Basolateral
    • Na+/K+ ATPase
    • K+ channel
53
Q

What are the EKG effects of hyperkalemia?

A

As hyperkalemia progresses, the following ECG chagnes appear:

  • High T wave
  • Prolonged PR interval, depressed ST segment
  • Ventricular fibrillation

Renal by Minnie (27 decks)

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