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38 Cards in this Set

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What is the definition of a metabolic alkalosis?
An increase in both serum pH and HCO3. (pH > 7.45)
An increase in both serum pH and HCO3. (pH > 7.45)
What happens in the generation phase of a metabolic alkalosis? (2 things)
"There is a:

1. Loss of acid: 
       Cl depletion (either with H+ or NH4+ loss, depending on route); 
        Depletion of K;
        ECF volume contraction.

2. Gain of bicarbonate.

"
There is a:

1. Loss of acid: 
       Cl depletion (either with H+ or NH4+ loss, depending on route); 
        Depletion of K;
        ECF volume contraction.

2. Gain of bicarbonate.
What happens during the maintenance phase of metabolic alkalosis? (3 things)
"1. There is a decrease in ECF volume,
    -increased bicarbonate reabsorption
    -decreased GFR
    -increase in serum aldosterone

2.  Decrease in K

3. Decrease in Cl"
1. There is a decrease in ECF volume,
    -increased bicarbonate reabsorption
    -decreased GFR
    -increase in serum aldosterone

2.  Decrease in K

3. Decrease in Cl
What are the two key components to a diagnostic approach to metabolic alkalosis?
The two components are:
Assessment of ECF volume;
Lab assessment.
What labs are most important in the assessment of metabolic alkalosis?  (3)
urine Cl
renin
aldosterone
What are the two general classifications of metabolic alkalosis?

Which is more common?
"1. Reduced ECF (typically Cl-responsive metabolic alkalosis)
2. Higher ECF (normovolemia or hypervolemia - typically Cl insensitive)

It's more common to have a Cl-responsive metabolic alkalosis."
1. Reduced ECF (typically Cl-responsive metabolic alkalosis)
2. Higher ECF (normovolemia or hypervolemia - typically Cl insensitive)

It's more common to have a Cl-responsive metabolic alkalosis.
What are three causes of  metabolic acidosis with decreased ECF volume?
"Vomiting
Diarrhea
Diuretics
Chloride-wasting disease (cystic fibrosis, chloride-wasting enteropathy)
Bartter's or Gitelman's syndrome (inherited tubular disorders)"
Vomiting
Diarrhea
Diuretics
Chloride-wasting disease (cystic fibrosis, chloride-wasting enteropathy)
Bartter's or Gitelman's syndrome (inherited tubular disorders)
What are 2 aetiologies of euvolemic or hypervolemic metabolic alkalosis?
"1. Processes that increase both circulating renin and aldosterone:
     -Malignant Hypertension
     -Renin tumours

2. Decreasing renin and increasing aldosterone
     -Primary hyperaldosteronism (Conn's syndrome)

3. Decreasing ...
1. Processes that increase both circulating renin and aldosterone:
     -Malignant Hypertension
     -Renin tumours
-Renal artery stenosis

2. Decreasing renin and increasing aldosterone
     -Primary hyperaldosteronism (Conn's syndrome)

3. Decreasing renin and aldosterone
    -Exogenous corticosteroids
    -Cushing's syndrome
    -Excessive licorice intake
In a patient with metabolic alkalosis, if the urine contains elevated sodium and potassium, but decreased chloride, what is a likely aetiology?
Recent vomiting.
Recent vomiting.
In a patient with metabolic alkalosis, if the urine contains elevated sodium and potassium and chloride, what is a likely aetiology if she is hypovolemic?

What if she's euvolemic?
"The patient could have recently taken a diuretic agent.

If euvolemic, it could also be diuretic use, or could also be due to an inherited tubular defect."
The patient could have recently taken a diuretic agent.

If euvolemic, it could also be diuretic use, or could also be due to an inherited tubular defect.
What are the three principal ways to treat metabolic alkalosis?
1. Repletion (most common treatment)
      a) Restore ECF volume
      b) Correct KCl or NaCl deficiencies

2.  Remove HCO3 (3 ways) (if alkalosis is life threatening)
     a) Increase renal secretion with acetazolamide
     b) Add IV HCl (rarely)
     c) Hemodialysis (in extreme cases)

3.  Treat specific conditions, if metabolic alkalosis is secondary.
What is the most important route for potassium excretion?

What organ is most responsible for potassium regulation in the body?
"Through the urine (95%).

The kidney, by controlling excretion."
Through the urine (95%).

The kidney, by controlling excretion.
What four factors can contribute to the formation of a real (or apparent) potassium disorder?
Pseudo-effects (i.e. pseudohyperkalemia: lab artifact where potassium leaks out of cells after blood sample taken)
Intake (either excessive intake or dietary potassium deficiency.  Rare as sole cause but may contribute with other factors.
Shift (i.e. from intracellular potassium into the ECF)
Excretion (in stool or urine)
What can cause a shift of potassium from the ECF into intact liver or skeletal muscle cells? (2 factors)

What causes a shift out?
"Stimulation of the beta-2 receptors or insulin receptors.


"
Stimulation of the beta-2 receptors or insulin receptors.

Stimulation of alpha receptors
Where is the majority of potassium resorption in the kidney performed?
"In the proximal tubule and the Loop of Henle (~90%).

What mechanisms are used to resorb the potassium at each of those two sites?"
In the proximal tubule and the Loop of Henle (~90%).
What controls the secretion of potassium by the principal cells of the collecting duct? (3 factors)
What controls the secretion of potassium by the principal cells of the collecting duct? (3 factors)
"In the Cortical Collecting Duct:
Flow of filtrate (and concentration of Na);
Number and function of luminal Na and K channels (impaired by K-sparing diuretics);
Activity  Na-K ATPases (affected by aldosterone)"
In the Cortical Collecting Duct:
Flow of filtrate (and concentration of Na);
Number and function of luminal Na and K channels (impaired by K-sparing diuretics);
Activity  Na-K ATPases (affected by aldosterone)
Name 2 ways that loop and thiazide diuretics stimulate the secretion of potassium into the urine.
"They decrease the ECF volume, which increases the amount of circulating aldosterone (which stimulates sodium resorption in the distal tubule).
They increase the volume of filtrate flow, increasing the amount resorbed by Principal cells.
They in...
They decrease the ECF volume, which increases the amount of circulating aldosterone (which stimulates sodium resorption in the distal tubule).
They increase the volume of filtrate flow, increasing the amount reabsorbed by Principal cells.
They increase the concentration of Na in the filtrate, driving more K secretion.
What other solutes in the filtrate can affect distal potassium secretion?
Name four drugs that reduce potassium secretion and their mechanism of action.
"Amiloride (K-sparing diuretic): blocks Na channel in principal cells.
Spironolactone: aldosterone antagonist.
Digitalis (toxic): inhibits Na-K ATPase.
NSAID: decreases GFR, inhibits Renin release."
Amiloride (K-sparing diuretic): blocks Na channel in principal cells.
Spironolactone: aldosterone antagonist.
Digitalis (toxicity): inhibits Na-K ATPase.
NSAID: decreases GFR, inhibits Renin release.
What does the transtubular potassium gradient (TTKG) estimate?

What four parameters do you need to calculate the  TTKG?"
"It measures the driving force for K excretion at the level of the Cortical Collecting Duct, i.e. asseses whether the aldosterone response is adequate.

TTKG is calculated from the urine potassium concentration and osmolality, and the serum pota...
It measures the driving force for K excretion at the level of the Cortical Collecting Duct, i.e. asseses whether the aldosterone response is adequate.

TTKG is calculated from the urine potassium concentration and osmolality, and the serum potassium concentration and osmolality.

What values do you expect for a hyperkalemic patient?
Hypokalemic?
What values for the TTKG do you expect for a hyperkalemic patient?

Hypokalemic?
Hyperkalemic > 8

hypokalemic < 3
What features on an ECG suggest hyperkalemia? (name 2)
"Peaked T-waves,
Small or absent P-waves,
QRS prolongation,
Conduction blocks."
Peaked T-waves,
Small or absent P-waves,
QRS prolongation,
Conduction blocks.
What gastrointestinal symptoms might a patient with hyperkalemia exhibit? (2)

What neuromuscular symptoms?
GI: 1) Nausea and vomiting, 2) Abdominal pain.

NM: 1) Weakness, 2) Paresthesia, 3) Ascending paralysis, 4) Quadraplegia.
Name four things you need to assess in evaluating a patient with hyperkalemia.
Assess for:
Cause(think pseudo, intake, shift);
Identify causes for shift (between ECF and ICF) and Offending drugs;
ECF volume and Renal function;
TTKG.;
Name four potential causes of pseudohyperkalemia.
Pseudohyperkalemia is caused by cells rupturing or leaking potassium after a blood sample's been drawn.  It can be induced by a number of conditions:
Pseudohyperkalemia is caused by cells rupturing or leaking potassium after a blood sample's been drawn.  It can be induced by a number of conditions:
What might cause hyperkalemia induced by shifting potassium from the ICF to the ECF? (give 4)
Any drug or hormonal factor that causes potassium to be secreted from the cells, or any process where cells are damaged. (see list)
Any drug or hormonal factor that causes potassium to be secreted from the cells, or any process where cells are damaged. (see list)
Name three factors that can contribute to hyperkalemia due to reduced renal secretion of potassium.
Factors that might cause a reduction in GFR (ACEi, NSAIDs)
Factors that might cause a reduction in tubular flow.
Factors that decrease the amount of potassium secreted by the Principal Cells. (Tubulointerstitial Nephritis, Obstructive neuropathy, or an Aldosterone problem).
What are the three most important considerations in treating a patient with hyperkalemia?
1) Ensure ABCs are not compromised; fluid resuscitate if dehydrated.

2) Protect heart from effects of hyperkalemia:
     -Calcium gluconate or calcium chloride (1-2 amps) reduces the excitability of myocytes, protecting from arrhythmias.

3) Shift K from ECF into cells:
     -IV glucose and insulin
     -Beta agonist (ventolin or albuterol)
     -Bicarbonate
What are some methods for longer term eliminating potassium out of the ECF in hyperkalemic patients? (3)
1) Diuretics can increase the amount of potassium that is filtered and excreted.

2) Dialysis is the most rapid way to remove excess potassium from the serum, but is used only in extreme cases.

3) Cation exchange resins bind with potassium in the gut and prevent absorption.
      -e.g. Resonium Calcium and Resonium Sodium (kayexalate)
What ECG changes might you see in a patient with hypokalemia? (give 2)
"1) Characteristic U-wave;
2) T wave flattening,
3) Atrial or ventricular tachyarrhytmias,
4) ST depression and T wave flattening,
5) Prolonged QT interval."
1) Characteristic U-wave;
2) T wave flattening,
3) Atrial or ventricular tachyarrhytmias,
4) ST depression and T wave flattening,
5) Prolonged QT interval.
6) U waves
What symptoms or findings might a patient with hypokalemia present with? (give 3)
1) Muscle weakness;
2) Palpitations;
3) Hypertension;
4) Worsening DM control;
5) Polyuria.
How is the diagnostic approach to hypokalemia different from hyperkalemia?

and what is an appropriate TTKG?
"In addition to estimating ECF volume and renal function and calculating TTKG, as you would for hyperkalemia, you may have to:
    1) Perform spot urines to assess changes with vomitting or diuretic use.
    2) Perform 24 hour urine test for...
In addition to estimating ECF volume and renal function and calculating TTKG, as you would for hyperkalemia, you may have to:
    1) Perform spot urines to assess changes with vomitting or diuretic use.
    2) Perform 24 hour urine test for aldosterone.
    3) Perform CT or MRI imaging of adrenals.

Appropriate TTKG for hypokalemia is < 3
What are the three ways that hypokalemia can develop (categorically)?
1) Dietary potassium deficiency (rarely)
2) Shift from ECF into cells.
3) Increased secretion (either through GI, or more commonly through urine)
What are three causes of a shift of potassium from the ECF into cells that can result in hypokalemia?
1) Metabolic alkalosis: excess bicarbonate drives K into cells.
2) Insulin excess; (e.g. DM2),
3) Beta agonist, (e.g. trauma),
4) Hypokalemic periodic paralysis,
5) Barium or chloroquine intoxication,
6) Hypothermia.
In what two ways do GI losses typically lead to the development of hypokalemia? (upper and lower)
Lower GI: simply by way of sustained loss of potassium.

Upper GI: renal secretion secondary to a metabolic alkalosis.
Give three examples of causes of renal excretion of potassium that can lead to a hypokalemia.
1) Secondary to metabolic alkalosis.
2) An excess of non-absorbable anions
     -their presence in the proximal tubule leads to decreased sodium reabsorption, increasing potassium secretion in the Primary cells.

3) Diuretic use
     -Especially loop and thiazide diuretics
     -Acetezolamide (increases bicarbonate secretion)
4) Salt wasting states (Chronic tubular interstitial nephritis (TIN));
5) Hypomagnesemia;
6) Very high urine flow rates.
7) Hyperaldosteronism
8) Exogenous mineralcorticoids (licorice)
Give three causes for hyperaldosteronism.
1) Primary hyperaldosteronism,
2) Adrenal hyperplasia,
3) Adrenal adenoma,
4) Adrenal carcinoma,
5) Renal artery stenosis.

The effects of hyperaldosteronism on potassium secretion can be mimicked my elevated cortisol levels (Cushing's syndrome) or even normal levels in the presence of glycyrrhizic acid (from liquorice).
What are three principals in the treatment of hypokalemia?
1) Treat the underlying problem (i.e reduce gastric acid secretion, correct volume, correct Mg deficiency).

2) Use potassium-sparing diuretics.

3) Replace potassium: not more than 20 mEq/hr.
If your patient has a plasma K of 2.5 mM, how much potassium should you administer to correct his hypokalemia?
About 400 mEq.
About 400 mEq.