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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
Describe the mechanism for K+ reabsorption in the proximal tubule
Paracellular pathway H2O is reabsorbed and K+ comes with ti This reabsorbs about 67% of filtered K+
26
What are the common causes of iatrogenic renal hyperkalemia?
* **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
What are the EKG effects of hypokalemia?
As hypokalemia worsens, the following EKG changes appear: * Low T wave * High U wave * Low ST segment
28
What stimulus drives K+ secretion through ROMK?
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
How can you tell whether a patient has Bartter’s syndrome or is taking secret loop diuretics?
* Bartter’s and Gitelman’s -\> low magnesium (But not conclusive) * Genetic analysis
30
How does metabolic acidosis affect K+ homeostasis?
Metabolic acidosis **increases plasma K+** Acidosis -\> * Inhibition of the Na+/K+ ATPase * Activation of the ATP-sensitive K+ channels
31
How does exercise affect K+ homeostasis?
Exercise causes the release of K+ from skeletal muscle cells, resulting in **increased plasma K+**
32
What is the effect of hypokalemia on the heart?
Hypokalemia hyperpolarizes the myocyte (more negative membrane potential) It is **less likely to fire an action potential**
33
Why might plasma K only be slightly reduced even with substantial body K+ depletion?
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
The intracellular concentration of K+ is ______ mEq/L The extracellular concentration of K+ is ______ mEq/L
The intracellular concentration of K+ is **_150_** mEq/L The extracellular concentration of K+ is **_4_** mEq/L
35
Which proteins in the principal cells of the cortical collecting duct are responsible for the secretion of K+?
* **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 ## Footnote *\*\*The Na+ channel is more important than the K+ channel in the regulation of K+ secretion!\*\**
36
What diseases might produce hypokalemia associated with hypertension?
* Primary hyperaldosteronism * Cushings syndrome
37
What is the first EKG manifestation of hypokalemia?
Low T wave
38
What is the difference between depletional hypokalemia and nondepletional hypokalemia?
* 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
How does metabolic alkylosis affect K+ homeostasis?
Metabolic alkylosis **decreases plasma K+** * Activation of the Na+/K+ ATPase * Inhibition of the ATP-sensitive K+ channels
40
How does aldosterone affect K+ homeostasis?
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
What is the effect of hyperkalemia on the heart?
Hyperkalemia depolarizes the myocyte (membrane potential becomes less negative) This makes the cell **more excitable, and more likely to fire an action potential**
42
What causes Gitelman’s syndrome? What is the effect on K+ homeostasis?
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
What causes Bartter’s syndrome? How does it affect K+ homeostasis?
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
How does increased plasma osmolality affect K+ homeostasis?
Increased osmolality -\> **Increased plasma K+** Increased plasma osmolality shifts water out of the cell, **dragging K+ along with it**
45
What are the major causes of hypokalemia due to abnormal transcellular distribution of potassium? (Non-depletional hypokalemia)
* Excess insulin * Beta-adrenergic agonists (albuterol) * Acute illness * Alkalemia All stimulate the Na+/K+ ATPase
46
Why would you suggest that Type I diabetics eat a low-potassium diet?
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
What happens to your plasma K+ concentration if you consume too much potassium in your diet?
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
What are the most dangerous effects of inhibition of the Na+/K+ ATPase?
Hyperkalemia -\> Death
49
Why might it be dangerous to give an ACE inhibitor to a patient with renal failure?
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
How do beta-blockers affect K+ homestasis?
Beta blockers can cause hyperkalemia Inhibition of the Na+/K+ ATPase
51
Why does aldosterone deficiency result in hyperkalemia?
* No aldosterone * -\> cannot increase Na+ reabsorption * -\> K+ secretion does not increase * -\> Hyperkalemia
52
Decribe the mechanism for K+ reabsorption in the thick ascending limb of the Loop of Henle
* Apical * K+/Na+/2Cl- cotransporter * More active than the ROMK K+ channel for secretion * Basolateral * Na+/K+ ATPase * K+ channel
53
What are the EKG effects of hyperkalemia?
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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