9/14- Dyskalemias Flashcards
What can cause hyperkalemia?
- Rhabdomyolysis
- Hemolysis
Pseudo-hypokalemia (no lysis)?
AML
- Abnormal WBC
- Numerous WBC
- Prolonged standing
- Consumption of extracellular K
[rapid separation of plasma or store at 4’C]
Pseudo-hyperkalemia (no lysis)
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]
What may cause hypokalemia?
- Sympathomimetics: Beta stimulants [asthma, premature labor], pain
- Alkalosis / Alkalemia
- Periodic paralysis
- Excess Insulin
- Rapid cell production: Lymphomas, leukemias, GM-CSF, B12 therapy, anabolic states
What may cause hyperkalemia?
Sympathetic blockers
- Betablockers
- Scoline
Inorganic Acidosis / Acidemia
Osmolality high
Insulinopenia
Rapid cell destruction
- Rhabdomyolysis
- In vitro hemolysis etc
- Tissue necrosis
Kidney determinants of K handling
- Distal Na delivery (Na/K exchange)
- RAAAS
- ENaC (epithelial Na channel)
What increases/decreases ENaC activity?
What are the effects of this?
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
What increases function of Na-K-ATPase?
Aldosterone
Learn this ion transport activity of principal cell
- ENaC stmulation -> Na retention (and HTN)
- ENaC inhibition -> hyperkalemia
What may cause an 11B hydroxysteroid dehydrogenase block?
What does this enzyme do?
This enzyme is responsible for converting cortisol into cortisone (prevents formation of final glucocorticoid?)
- Apparent mineralocorticoid excess
- Licorice (glycyrrhetinic acid)
How will pts with an 11B hydroxysteroid dehydrogenase block present?
Severe hypokalemia
- Severe volume overload (S3 gallop…)
When are renin levels increased? decreased?
Increased:
- Malignant HTN
- Renovascular HTN
- Renin producing tumor
- Volume depletion
Decreased:
- Beta blockers
When are ang II levels/receptor decreased/inhibited?
- ACE inhibitors
- A-II receptor blockers (ARCBs)
When are aldosterone levels increased? decreased?
Increased:
- Adrenal adenoma
- Adrenal hyperplasia
Decreased:
- Adrenal insufficiency
- Heparin
- NSAIDs
When are aldo receptor levels increased? decreased?
Increased:
- Non aldosterone hormones: glucocorticoids, cortisol, ectopic ACTH
- Congenital adrenal hyperplasia
Decreased:
- Sprinolocatone
- Eplerenone
When are ENaC levels increased? decreased?
Increased:
- Aldosterone
- Liddle’s syndrome
Decreased:
- Amiloride
- Triamterene
- Trimethoprim
- Pentamidine
What may cause hypokalemia?
Will have hypokalemia and HTN
- Increased renin
((- Increased angi II/receptor: nothing does this directly))
- Increased aldosterone
- Increased aldosterone receptor
- Increased ENaC
What may cause hyperkalemia?
- Decreased renin
- Dereased angi II/receptor
- Decreased aldosterone
- Decreased aldosterone receptor
- Decreased ENaC
What is seen clinically in patients with hypokalemia?
Asymptomatic lab abnormality in 20% of inpts
Muscle weakness
- Cardiac: ventricular arrhythmias
- Skeletal: weakness, cramping, myalgias, paralysis
Paralysis
Sudden death
What is the first question to consider in hypokalemic state?
Is the urine K greater or less than 20 mEq/day
(Is kidney trying to dump or conserve?)
If urine K is under 20 mEq/day, what does that indicate for hypokalemia?
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
If urine K is > 20 mEq/day, what do you need to consider?
See if BP is high
- If hypokalemic and hypertensive, need to look at the RAAAS system
What do different levels of renin and aldosterone indicate for pt who is hypokalemic and hypertensive?
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
If pt is hypokalemic and blood pressure is normal/low, what must be considered?
See if serum HCO3 is low or high
If pt is hypokalemic and blood pressure is normal/low, what does low HCO3 indicate?
RTA
If pt is hypokalemic and blood pressure is normal/low, what does high HCO3 indicate?
Need to see if urine Cl is low or high
What could cause: hypokalemia with normal/low BP, high HCO3 and low urine Cl?
Nonreabsorbable anion (carbenicillin, ketoanion, HCO3)
What could cause: hypokalemia with normal/low BP, high HCO3 and high urine Cl?
- Diuretics (loop and thiazide)
- Osmotic diuresis
- Bartter’s
- Gitelman’s
How do loop and thiazide diuretics contribute to hypokalemia with high urine Cl?
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
Key flowchart
Distinguishing characteristics for:
- Gitelman’s
- Barrter’s
- Liddle’s
- Hypocalciuria in Gitelman’s
What is hypokalemic periodic paralysis?
- 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:
- AD, mutation in alpha-1 subunit DHP-sensitive Ca channel
- Thyrotoxicosis: Asians and Mexicans
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
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
If both renin and aldosterone levels are low in patient with:
- Hypokalemia
- HTN
- Alkalosis
- High urine K
What is your diagnosis? Treatment?
Most likely Liddle’s Syndrome
- ENaC channel always open!
Treatment: Amiloride (blocks ENaC channel)
What ECG changes occur with hypokalemia?
- Slightly peaked P wave
- Slightly prolonged PR interval
- ST depression
- Shallow T wave
- Prominent U wave
Treatment for various hypokalemic states
Must give K via infusion
- Don’t exceed 10-15 mEq/hour or you can cause severe arrhythmias!
- Don’t give in dextrose!
Potassium replacement strategies
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…
What other deficiency is commonly associated with hypokalemia?
How can this be treated?
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
What can cause hyperkalemia?
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
What are common drugs causing hyperkalemia?
- K sparing diuretics
- NSAID/COX2 inh
- Cyclosporine
- Tacrolimus
- Heparin
- ACEI
- ARB
- Pentamidine
- Trimethoprim
Less common:
- Beta blockers
- Digitalis (block Na-K-ATPase in muscles)
- Succinylcholine (K release from cells)
- Lithium poisoning
What EKG changes are seen with hyperkalemia?
- 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
Treatment of hyperkalemia?
Antagonize cardiac effects
- Calcium
Shift intracellularly
- Insulin and dextrose
- NaHCO3
- Beta2 stimulants
K removal
- Lasix/mineralocorticoids (Fludrocortisone)
- Cation exchange resin
- Dialysis
Mechanism/details of using Ca to treat hyperkalemia
- Mechanism
- Dosage
- Effects
- Consider
- 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
Mechanism/details of using insulin and dextrose to treat hyperkalemia
- Dosing
- Timeline
- Specific situations
- 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
Mechanism/details of using sodium bicarbonate to treat hyperkalemia
- Effective when
- Uses
- Consider
- Effective only if severe acidemia +
- Improves efficacy of Insulin in acidemia
- Not useful routinely
- AVOID in CHF pts (huge Na load)
Mechanism/details of using Beta2 adrenergic agonists to treat hyperkalemia
- Uses
Inconsistent K+ lowering effect and tachyarrthymias : not routinely used
Mechanism/details of using cation exchange resin (kayexalate) to treat hyperkalemia?
- Relationship between resin/K
- Accompanying treatments
- Route of administration
- Complication
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
