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Renal Week 2 > Lecture 17: Disorders of Potassium Balance, Hyperkalemia > Flashcards

Lecture 17: Disorders of Potassium Balance, Hyperkalemia Flashcards

1
Q

What are the key characteristics of hyperkalemia?

A 
Hyperkalemia > 5 mEq/L
Can be acute or chronic
Can present in three ways
	i. normal total body K content
	ii. high K body content
	iii. low K body content
Can be iatrogenic and fatal
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2
Q

What are the key factors that regulate K internal balance?

A
  1. Insulin
  2. Catecholamines
  3. Aldosterone
  4. Posm
  5. Acid-base status
  6. Na/K ATPase
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3
Q

Why is hyperkalemia a problem?

A

Gain of ICF K = cell swelling = cell alkalosis (since K and H always interchange)
More ICF K = more inactivation gates closed for Na (since membrane potential is depolarized)
Can lead to muscle excitability
Hyperkalemia also leads to conduction issues in the heart
Hyperkalemia can also lead to vasodilation of SMCs

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4
Q

What are the clinical manifestations of hyperkalemia?

A
  1. ECG changes and cardiac arrhythmias
  2. Muscle weakness, paralysis
    -cells depolarize
    -increased membrane excitability initially
    But Then
    -persistent depolarization reduces membrane excitability due to Na channel inactivation
  3. Paresthesia
  4. Impaired urinary acidification
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5
Q

What are the ECG manifestatiosn of hyperkalemia?

A

Peaked T waves (V2-V4)
Prolonged PR interval
Flattening or absence of p waves (the greater the hyperkalemia)
Wider QRS complex
Severe hyperkalemia ECG abnormalities evolve within seconds
Correlation between K levels and ECG is imprecise

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6
Q

What are the causes of hyperkalemia?

A
  1. Too much K intake
  2. Too little K excretion
  3. lysis of cells which release K into the ECF
    Usually patients have defect in at least 2 of these factors
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7
Q

What is pseudohyperkalemia?

A

When potassium levels are elevated due to release of K from cells either during or after blood specimen is obtained in ABSENCE of true elevated serum K concentration
Serum concentration collected after the blood clots
However, if serum is put on the slide too rapidly or is roughly handled, can cause RBC and WBC after blood is drawn from person
-this leads to elevated SERUM K concentration, but there is a normal PLASMA K concentration

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8
Q

What are causes of pseudohyperkalemia?

A
  1. In vitro hemolysis
  2. Leukocytosis (WBC>70,000/cm^3)
    • plasma K normal but serum K is high
  3. Thrombocytosis (platelet count > 500,000cm^3)
    • plasma K normal but serum K is high
  4. Fist-clenching during blood drawing (isn’t this what I do all the time?) if arm is wrapped in a tourniquet…breakdown of muscle?
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9
Q

What are the characteristics of hyperkalemia due to excessive intake?

A

Excessive K intake alone is almost never the cause alone
Can only cause more than mild transient hyperkalemia if there is impairment of K excretion in the other two causes
If you do want to cause hyperkalemia, then you have to have chronic K intake
That is because distal tubule can secrete crapload of K from collecting tubule

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10
Q

What are the most common dietary sources of hyperkalemia?

A
  1. potatoes, avocados, cantaloupe, bananas, oranges, fruit juices, tomatoes
  2. salt substitute
  3. health food/nutritional supplements
  4. parenteral nutrition/enteral feedings (iatrogenic)
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11
Q

What is recommended daily potassium intake?

A

4,500 mg per day

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12
Q

What are the most common medications that can cause hyperkalemia?

A
  1. K supplement (KCl)
  2. Polycitra-K: 2 mEq/ml
  3. Neutra-Phos/Neutra-phos-K: 7-14 mEq/dose
  4. Potassium penicillin: up to 41 mEq/daily dose
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13
Q

What are the characteristics of hyperkalemia due to too little excretion?

A
  1. Low GFR
    • acute kidney injury (AKI)
    • chronic renal disease (CKD)
  2. Impaired RAA axis
  3. Inadequate distal Na delivery and urine
    • reduced aldosterone synthesis
    • reduced responsiveness to aldosterone
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14
Q

What are conditions that lead to low GFR (and thus hyperkalemia?

A
  1. acute kidney injury (AKI)

2. Chronic renal disease (CKD)

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15
Q

What is the difference between acute and chronic kidney disease with relation to hyperkalemia?

A 
Acute = compensatory mechanisms don’t have time to kick in yet
Chronic = already compensation in terms of tubular hyperplasia of principal cell BLM area, increase Na/K atpase activity and increased apical K channel activity
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16
Q

What are the conditions that lead to RAAS impairment?

A
  1. Reduced aldosterone synthesis

2. Reduced responsiveness to aldosterone

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17
Q

What are the potential causes of reduced aldosterone synthesis?

A
  1. Addison’s disease (adrenal insufficiency)
  2. Genetic disorders
    -Congenital adrenal hyperplasia
    -Aldosterone synthase mutations
  3. Type IV RTA with hypreninemic hypoaldosteronism
  4. Drugs like NSAIDs, ACEi and ARBs, cyclosporine, tacrolimus, heparin
    MoA slide 12 of lecture
  5. HIV, Tb, fungal infections, infarction can also mess with adrenals
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18
Q

What does RTA stand for?

A

Renal Tubular Acidosis

Involves accumulation of acid due to failure of kidneys to appropriately acidify the urine

19
Q

What is pseudohypoaldosteronism (PHA)?

A

When distal nephron is poorly responsive to aldosterone due to genetic reasons
Thus, lack of aldosterone response is NOT due to lack of aldosterone in the body
PHA1 = due to defect in ENaC or Mineralocorticoid receptor
PHA2 = gordon’s syndrome = dysfunction of kinase system that regulates Na-Cl symporter in DCT

20
Q

What are the causes of impaired aldosterone responsiveness?

A
  1. Drugs
  2. Tubulointerstitial kidney disease (will be covered later)
    Ie drug induced interstitial nephritis, kidney transplant rejection, etc
  3. Pseudohypoaldosteronism
  4. Anything that scars the collecting duct
21
Q

What drugs impair aldosterone responsiveness?

A
  1. Amiloride (direct ENaC inhibitor)
  2. Spironolactone and Eplerenone (MR antagonists)
  3. Triamterene, trimethoprim, pentamidine (ENaC inhibitors too)
    Thus these drugs are common causes of hyperkalemia
22
Q

What is Trimethoprim used for?

A

Antibiotic used with Sulfamethoxazole to treat Pneumocystis jirovecii
Can cause HYPERkalemia

23
Q

What are acute causes of abnormal internal balance leading to hyperkalemia?

A
  1. insulin deficiency
  2. hypertonicity
  3. metabolic acidosis
  4. drugs
  5. exercise
  6. muscle necrosis and cell lysis
  7. Hyperkalemic periodic paralysis
    • intermittent episodes of acute translocation of K from ICF to ECF
24
Q

How can digoxin lead to hyperkalemia?

A

By blocking Na/K pump, so potassium stays in plasma

25
Q

What are causes of rhabdomyolysis?

A

When alscoholics or drug users sleep on hard surfaces, causing ischemic pressure injury to muscle
Also can be caused by cocaine and ecstasy, malignant hyperthermia, hypophosphatemia, and extreme exertion, trauma

26
Q

What are the characteristics of hyperkalemic periodic paralysis?

A

Intermittent episodes of acute translocation of K from ICF to ECF
Rare disorder

27
Q

What happens to plasma K when one fasts?

A

Plasma K increases because there is no insulin to secrete K (or activate Na/K) as one is fasting

28
Q

What happens to plasma K when one adds effective osmoles?

A

Effective osmoles = mannitol, glucose, NaCl, NaHCO3
Adding effective osmoles that stay on the ECF side of things will draw K from ICF to ECF
Due to:
i. solvent drag
ii. paracellular diffusion due to inherent increased K concentration (because water is being lost, thereby further concentrating K+)

29
Q

What is the relationship between blood glucose levels and hyperkalemia?

A

The more glucose in blood = greater plasma K concentration

Seen in DKA and hyperosmolar, hyperglycemic non-ketotic (HHNK) syndrome

30
Q

What is the effect of metabolic acidosis on hyperkalemia?

A

Acute metabolic acidosis can cause TRANSIENT hyperkalemia

Mechanism: increased ECF H+ will enter the cell and K+ will diffuse out to compensate

31
Q

What is the difference between HCl and beta hydroxybutyric acid (B-OH-B) on K secretion to ECF?

A

HCl infusion into portal vein does NOT induce insulin secretion so there is high level of K acutely
B-OH-B on the other hand does upregulate insulin secretion so there will be an increase in K secretion, thus a decrease in plasma K concentration

32
Q

How does one evaluate patient with hyperkalemia?

A

With TransTubular Potassium (K) Gradient (TTKG)
TTKG = [urineK/plasmaK]/(Uosm/Posm)
TTKG used to assess K secretion by collecting duct and urinary K excretion

33
Q

What is the greatest utility of TTKG?

A

Can tell the difference between hypoaldosteronism or aldosterone resistance
TTKG > 6 after MR administration suggests hypoaldosteronism with normal responsiveness
TTKG < 6 after MR administration suggests either hypoaldosteronism and/or aldosterone resistance
TTKG normally = 7-10 and is usually >10 as K secretion increases

34
Q

What is the emergency treatment for severe acute hyperkalemia?

A
  1. Antagonize cardiac (ECG) effects
  2. Move K from the ECF into cells
  3. Remove K from the body
35
Q

How does on antagonize the cardiac effects?

A
  1. calcium gluconate
    -MoA not clear, but it increases threshold potential at which excitation occurs
    -increases number of membrane Na channels resulting in faster conduction
    Thus you need to use calcium to counteract ECG effects of hyperkalemia
    -calcium infusion does NOTHING to serum K
    Calcium infusion makes the threshold for action potential higher, so greater separation between resting membrane potential of K and what is necessary depolarization
36
Q

How does one move K into the cells as part of hyperkalemia treatment?

A
  1. Insulin
  2. B2 agonists
  3. sodium bicarbonate
37
Q

How does insulin help move K into cells?

A

Stimulates muscle and liver cell uptake of K

MoA: insulin stimulation of Na/K ATPase

38
Q

How does B2 agonists move K into cells?

A

Increase cellular uptake of K by stimulation of Na/K ATPase in muscle and liver
Example: nebulized albuterol (for asthma)
MoA: stimulation of Na/K ATPase

39
Q

How does sodium bicarb move K into cells?

A

As more bicarb is in the ECF, more H+ will exit the cell to combine with HCO3-
Thus, the H+ efflux will upregulate K+ influx
Only effective in severe metabolic acidosis
Thus is NOT normally used

40
Q

How does one remove K from system?

A
  1. Loop diuretics
  2. Cation exchange resin-sodum polystyrene sulfonate
    Kayexalate
  3. Hemodialysis
41
Q

How do loop diuretics remove K from system?

A

Blocks NKCC2 so less K uptake in TAL
Only increases urinary K excretion if and only if ECF volume and urine output is maintained
Response to loop diuretics is variable
Thus do not use loop diuretic for acute cases
Only use loop diuretic for CHRONIC management of chronic hyperkalemia

42
Q

How does loop cation exchange resin remove K from system?

A

Aka Kayexalate
Resin binds K (and Ca and Mg) in exchange for Na
Administered orally with sorbitol (to forestall constipation) or as retention edema
Onset of action: 1-2 hours

43
Q

How does hemodialysis remove K from system?

A

Can remove 60-120 mEq K during a 4 hour treatment
So it is most effective for patients with severe hyperkalemia
Used when patient has significant renal failure, so increasing urinary K excretion is not an option

44
Q

How does one manage chronic hyperkalemia?

A
  1. Diuretics
  2. Kayexalate
  3. Reduce intake
  4. Review medications
  5. Increase Na intake (NaCl and NaHCO3)
  6. Fludrocortisone

Renal Week 2 (12 decks)

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