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MS2 Renal > 9/14- Dyskalemias > Flashcards

9/14- Dyskalemias Flashcards

1
Q

What can cause hyperkalemia?

A
  • Rhabdomyolysis
  • Hemolysis
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2
Q

Pseudo-hypokalemia (no lysis)?

A

AML

  • Abnormal WBC
  • Numerous WBC
  • Prolonged standing
  • Consumption of extracellular K

[rapid separation of plasma or store at 4’C]

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3
Q

Pseudo-hyperkalemia (no lysis)

A

Pseudo-hyperkalemia (no lysis)

  • Leukocytosis [> 70K/mm]
  • Thrombocytosis [>7.5e5/mm3)
  • Test tube hemolysis
  • Ischemic blood draw

[serum vs. plasma K: send sample in heparinized tube]

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4
Q

What may cause hypokalemia?

A

- Sympathomimetics: Beta stimulants [asthma, premature labor], pain

- Alkalosis / Alkalemia

- Periodic paralysis

- Excess Insulin

- Rapid cell production: Lymphomas, leukemias, GM-CSF, B12 therapy, anabolic states

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5
Q

What may cause hyperkalemia?

A

Sympathetic blockers

  • Betablockers
  • Scoline

Inorganic Acidosis / Acidemia

Osmolality high

Insulinopenia

Rapid cell destruction

  • Rhabdomyolysis
  • In vitro hemolysis etc
  • Tissue necrosis
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6
Q

Kidney determinants of K handling

A
  • Distal Na delivery (Na/K exchange)
  • RAAAS
  • ENaC (epithelial Na channel)
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7
Q

What increases/decreases ENaC activity?

What are the effects of this?

A

Increased epithelial Na channel:

  • Aldosterone
  • Liddle’s syndrome

Decreased epithelial Na channel:

(K sparing diuretics- block this channel to cause hyperkalemia)

  • Amiloride
  • Triamterene
  • Trimethoprim

ENaC stimulation -> Na retention (and HTN)

ENaC inhibition -> hyperkalemia

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8
Q

What increases function of Na-K-ATPase?

A

Aldosterone

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9
Q

Learn this ion transport activity of principal cell

A
  • ENaC stmulation -> Na retention (and HTN)
  • ENaC inhibition -> hyperkalemia
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10
Q

What may cause an 11B hydroxysteroid dehydrogenase block?

What does this enzyme do?

A

This enzyme is responsible for converting cortisol into cortisone (prevents formation of final glucocorticoid?)

  • Apparent mineralocorticoid excess
  • Licorice (glycyrrhetinic acid)
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11
Q

How will pts with an 11B hydroxysteroid dehydrogenase block present?

A

Severe hypokalemia

  • Severe volume overload (S3 gallop…)
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12
Q

When are renin levels increased? decreased?

A

Increased:

  • Malignant HTN
  • Renovascular HTN
  • Renin producing tumor
  • Volume depletion

Decreased:

  • Beta blockers
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13
Q

When are ang II levels/receptor decreased/inhibited?

A
  • ACE inhibitors
  • A-II receptor blockers (ARCBs)
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14
Q

When are aldosterone levels increased? decreased?

A

Increased:

  • Adrenal adenoma
  • Adrenal hyperplasia

Decreased:

  • Adrenal insufficiency
  • Heparin
  • NSAIDs
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15
Q

When are aldo receptor levels increased? decreased?

A

Increased:

  • Non aldosterone hormones: glucocorticoids, cortisol, ectopic ACTH
  • Congenital adrenal hyperplasia

Decreased:

  • Sprinolocatone
  • Eplerenone
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16
Q

When are ENaC levels increased? decreased?

A

Increased:

  • Aldosterone
  • Liddle’s syndrome

Decreased:

  • Amiloride
  • Triamterene
  • Trimethoprim
  • Pentamidine
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17
Q

What may cause hypokalemia?

A

Will have hypokalemia and HTN

  • Increased renin

((- Increased angi II/receptor: nothing does this directly))

  • Increased aldosterone
  • Increased aldosterone receptor
  • Increased ENaC
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18
Q

What may cause hyperkalemia?

A
  • Decreased renin
  • Dereased angi II/receptor
  • Decreased aldosterone
  • Decreased aldosterone receptor
  • Decreased ENaC
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19
Q

What is seen clinically in patients with hypokalemia?

A

Asymptomatic lab abnormality in 20% of inpts

Muscle weakness

  • Cardiac: ventricular arrhythmias
  • Skeletal: weakness, cramping, myalgias, paralysis

Paralysis

Sudden death

20
Q

What is the first question to consider in hypokalemic state?

A

Is the urine K greater or less than 20 mEq/day

(Is kidney trying to dump or conserve?)

21
Q

If urine K is under 20 mEq/day, what does that indicate for hypokalemia?

A

Non-renal cause (kidney is not dumping K!)

Lower GI losses

  • Diarrhea
  • Fistula

Upper GI (NG suction/vomiting): variable urine K

  • Lower urine K: alkalosis; intracellular shift
  • Normal or high urine K:

—- bicarbonaturia increases K loss

—- loss of Na causes 2ndary stimulation of aldosterone

22
Q

If urine K is > 20 mEq/day, what do you need to consider?

A

See if BP is high

  • If hypokalemic and hypertensive, need to look at the RAAAS system
23
Q

What do different levels of renin and aldosterone indicate for pt who is hypokalemic and hypertensive?

A

High renin and high aldosterone:

  • RAS
  • Magignant HTN
  • Renin secreting tumor

Low renin but high aldosterone

  • Conn’s/adrenal adenoma
  • Bilateral cortical hyperplasia
  • GRA

Normal or low renin and angiotensin:

  • Cushing’s
  • Apparent mineralocorticoid excess
  • Congenital adrenal hyperplasia
  • Liddle’s
  • Mineralocorticoid receptor mutation
24
Q

If pt is hypokalemic and blood pressure is normal/low, what must be considered?

A

See if serum HCO3 is low or high

25
Q

If pt is hypokalemic and blood pressure is normal/low, what does low HCO3 indicate?

A

RTA

26
Q

If pt is hypokalemic and blood pressure is normal/low, what does high HCO3 indicate?

A

Need to see if urine Cl is low or high

27
Q

What could cause: hypokalemia with normal/low BP, high HCO3 and low urine Cl?

A

Nonreabsorbable anion (carbenicillin, ketoanion, HCO3)

28
Q

What could cause: hypokalemia with normal/low BP, high HCO3 and high urine Cl?

A
  • Diuretics (loop and thiazide)
  • Osmotic diuresis
  • Bartter’s
  • Gitelman’s
29
Q

How do loop and thiazide diuretics contribute to hypokalemia with high urine Cl?

A

Impair sodium and chloride reabsorption distal to PCT

  • High urine chloride
  • Loop diuretics: NKCC in Loop of Henle
  • Thiazides: NaCl transport in DCT

Results in increased distal sodium delivery to CCD

Volume depletion – secondary hyperaldo state

30
Q

Key flowchart

A
31
Q

Distinguishing characteristics for:

  • Gitelman’s
  • Barrter’s
  • Liddle’s
A
  • Hypocalciuria in Gitelman’s
32
Q

What is hypokalemic periodic paralysis?

A
  • Intermittent acute attacks of muscle weakness with hypokalemia (decreased phos and Mg often present)
  • Triggered by large CHO meals, rest post-exercise
  • 60-120 mEq K for acute attach then d/c
  • Beta2 blockade, cacetozolamide, decrease CHO diet, Rx increase thyroid state

Two forms:

  1. AD, mutation in alpha-1 subunit DHP-sensitive Ca channel
  2. Thyrotoxicosis: Asians and Mexicans
33
Q

Case)

  • 24 yo man
  • Intermittent weakness
  • Brother and father with HTN
  • P/E: normal except BP 140/106

Labs:

  • Na 145, K 2.8, Cl 97, CO2 32
  • ABG: pH 7.46, pCO2 42
  • Urinary K: 40 mEq/L

Overall:

  • Hypokalemia
  • HTN
  • Alkalosis
  • High urine K

What test is next?

A. Renin and aldosterone levels

B. Urine chloride

C. CT scan of abdomen to look at adrenal gland

D. Check thyroid function

A

What test is next?

A. Renin and aldosterone levels

B. Urine chloride

C. CT scan of abdomen to look at adrenal gland

D. Check thyroid function

34
Q

If both renin and aldosterone levels are low in patient with:

  • Hypokalemia
  • HTN
  • Alkalosis
  • High urine K

What is your diagnosis? Treatment?

A

Most likely Liddle’s Syndrome

  • ENaC channel always open!

Treatment: Amiloride (blocks ENaC channel)

35
Q

What ECG changes occur with hypokalemia?

A
  • Slightly peaked P wave
  • Slightly prolonged PR interval
  • ST depression
  • Shallow T wave
  • Prominent U wave
36
Q

Treatment for various hypokalemic states

A

Must give K via infusion

  • Don’t exceed 10-15 mEq/hour or you can cause severe arrhythmias!
  • Don’t give in dextrose!
37
Q

Potassium replacement strategies

A

KCl prep:

- IV: dispense in NS and NOT in dextrose; avoid > 20 mEq/hour

- Oral: diluted; GI irritation

Diet

  • Not useful adjuncts for replacement
  • 1 inch of banana = 1 mEq of K…
38
Q

What other deficiency is commonly associated with hypokalemia?

How can this be treated?

A

Hypomagnesemia (10-40% assoc w/ hypokalemia)

  • Occurs also with diuretics, DKA, alcoholism, ATN recovery, aminoglycoside toxicity, etc…

Treat:

  • MgO better than MgSO4 (latter induces kaliuresis)

Mechanism:

  • Mg blocks K channels
  • Increases K channel activity
  • Renal K wasting
39
Q

What can cause hyperkalemia?

A

Decreased GFR +/- excess intake

  • Acute or chronic kidney disease
  • Hidden sources

—- High dose PCN / citrate etc

—- Salt substitutes [~280 mEq / tablespoon]

—- Stored blood

—- Excess K replacement

Rhabdomyolysis / tissue trauma

Defect in Renin-Angiotensin- Aldosterone axis

  • Hypoaldosteronism
  • Type 4 RTA
  • Drugs like ACEI, ARB, Heparin, spironolactone etc
40
Q

What are common drugs causing hyperkalemia?

A
  1. K sparing diuretics
  2. NSAID/COX2 inh
  3. Cyclosporine
  4. Tacrolimus
  5. Heparin
  6. ACEI
  7. ARB
  8. Pentamidine
  9. Trimethoprim

Less common:

  • Beta blockers
  • Digitalis (block Na-K-ATPase in muscles)
  • Succinylcholine (K release from cells)
  • Lithium poisoning
41
Q

What EKG changes are seen with hyperkalemia?

A
  • Peaked T waves
  • Increased PR
  • Increased QRS
  • Flattening of P wave
  • Sine wave

Caveats:

  • Sensitivity of pt
  • Rapidity of hyperkalemia
  • Very unpredictable: does NOT march per degree of hyperkalemia
  • Can change from normal EKG to sine wave and death
42
Q

Treatment of hyperkalemia?

A

Antagonize cardiac effects

  • Calcium

Shift intracellularly

  • Insulin and dextrose
  • NaHCO3
  • Beta2 stimulants

K removal

  • Lasix/mineralocorticoids (Fludrocortisone)
  • Cation exchange resin
  • Dialysis
43
Q

Mechanism/details of using Ca to treat hyperkalemia

  • Mechanism
  • Dosage
  • Effects
  • Consider
A

- Mechanism: counteracts at membrane level; DOES NOT change K concentration

- Dosage: 10 mL of 10% Ca gluconate over 3 mins; repeat q5 min if ECG changes persist

- Effects: 30-60 min

- Consider: careful in pts on Digoxin

44
Q

Mechanism/details of using insulin and dextrose to treat hyperkalemia

  • Dosing
  • Timeline
  • Specific situations
A
  • 6-10 U of regular insulin IV + 50 g of glucose IV - 0.6
  • 1 mEq of fall in serum K
  • Takes 30-60 min for effect; starts at 15 min
  • Glucose not needed if severe hyperglycemia
45
Q

Mechanism/details of using sodium bicarbonate to treat hyperkalemia

  • Effective when
  • Uses
  • Consider
A
  • Effective only if severe acidemia +
  • Improves efficacy of Insulin in acidemia
  • Not useful routinely
  • AVOID in CHF pts (huge Na load)
46
Q

Mechanism/details of using Beta2 adrenergic agonists to treat hyperkalemia

  • Uses
A

Inconsistent K+ lowering effect and tachyarrthymias : not routinely used

47
Q

Mechanism/details of using cation exchange resin (kayexalate) to treat hyperkalemia?

  • Relationship between resin/K
  • Accompanying treatments
  • Route of administration
  • Complication
A

Sodium polysterene sulfonate

  • Gut: K+ exchanged for Na+
  • Relationship: 1 gm of Resin: Binds 1 mEq of K
  • Accompany with: Sorbitol to avoid constipation
  • Administration: Oral vs Enema

Intestinal Necrosis complication

  • If used within 1 wk after surgery
  • If given with sorbitol:

—- Post-surgery state: ileus leads to more contact with intestinal wall

—- Sorbitol directly damages mucosa

MS2 Renal (25 decks)

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