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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
If pt is hypokalemic and blood pressure is normal/low, what does low HCO3 indicate?
RTA
26
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
27
What could cause: hypokalemia with normal/low BP, high HCO3 and low urine Cl?
Nonreabsorbable anion (carbenicillin, ketoanion, HCO3)
28
What could cause: hypokalemia with normal/low BP, high HCO3 and high urine Cl?
- Diuretics (loop and thiazide) - Osmotic diuresis - Bartter's - Gitelman's
29
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
30
Key flowchart
31
Distinguishing characteristics for: - Gitelman's - Barrter's - Liddle's
- Hypocalciuria in Gitelman's
32
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:_ 1. AD, mutation in alpha-1 subunit DHP-sensitive Ca channel 2. Thyrotoxicosis: Asians and Mexicans
33
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
34
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)
35
What ECG changes occur with hypokalemia?
- Slightly peaked P wave - Slightly prolonged PR interval - ST depression - Shallow T wave - Prominent U wave
36
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!
37
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...
38
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
39
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
40
What are common drugs causing hyperkalemia?
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
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
42
Treatment of hyperkalemia?
**Antagonize cardiac effects** - Calcium **Shift intracellularly** - Insulin and dextrose - NaHCO3 - Beta2 stimulants **K removal** - Lasix/mineralocorticoids (Fludrocortisone) - Cation exchange resin - Dialysis
43
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**
44
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
45
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)
46
Mechanism/details of using **Beta2 adrenergic agonists** to treat hyperkalemia - Uses
Inconsistent K+ lowering effect and tachyarrthymias : not routinely used
47
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

MS2 Renal (25 decks)

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