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CPRII- Renal Exam > Electrolyte Disorders - Potassium > Flashcards

Electrolyte Disorders - Potassium Flashcards

1
Q

Primary regulator of serum K+

A

Kidney in the distal part of the nephron. Principle cells do secretion, and alpha-intercalated cells do reabsorption.

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2
Q

Difference between transcellular shift and renal excretion of K+

A

Shift is for immediate response and renal is for long-term

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3
Q

What drives K+ into cells?

A

B-adrenergic agonists: insulin, epi, aldosterone

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4
Q

What drives K+ out of cells

A

alpha-adrenergic agonists

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5
Q

Major intracellular cation is ___ and extracellular is ___

A

Intra: K
Extra: Na

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6
Q

What kind of K channel is in the thick ascending limb

A

NKCC2: K enters cell
ROMK: K leaves cell

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7
Q

What happens in the collecting duct in the principle cell?

A

Principle cells do K+ secretion
ENaC channel is here
Aldosterone acts here.

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8
Q

What happens in the collecting duct in the intercalated cell?

A

K+ reabsorption. K+/H+ antiporter is here.

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9
Q

What part of the nephron regulates urinary K+ secretion?

A

Distal part

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10
Q

Def. of hyperK and RFs

A

Serum K> 5 or 5.5 mEq/L

RFs: AKI, CKD, DM, Meds (NSAIDs, ARBs/ACEi, Aldosterone antags, heparin), malignancy, rhabdo, older pt, acidosis

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11
Q

Sx of hyperK

A
  • Cardiac arrhythmia (vfib, bradycardia due to AVB, asystole)
  • Skeletal muscle weakness (diaphragm!)
  • Metabolic acidosis
    1. too much K…K enters cells…so H+ leaves to try to keep neutrality…leads to ACIDOSIS!
    2. HperK decreases ammoniagenesis –> decreased ammonium chloride excretion in kidneys –> less net acid excretion
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12
Q

What does too much K+ do to the RMP?

A

Raises the RMP i.e. makes it LESS negative will increase excitability. Over time though, long-term depol. leads to Na channel deactivation, causing a net decrease in excitability. This is what causes cardiac and muscle issues.

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13
Q

What are some EKG findings in hyperK

A
  • Peaked T waves
  • Depressed ST
  • Prolonged QRS
  • Sinusoidal wave pattern (suggests vfib!)
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14
Q

What are the 2 main reasons for hyperK?

A
  1. Transcellular shift (K+ leaving cells)

2. Decreased renal K excretion

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15
Q

HYPOK: What can cause transcellular shifts of K+?

A
  • Insulin (DM, refeeding)
  • B2 agoinist (albuterol, catecholamines)
  • Metabolic alkalosis (lots of basic HCO3 in body so K+ leaves cells to maintain balance)
  • Pseudohypok
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16
Q

HYPOK: What can cause extrarenal loss of K+?`

A
  • Upper GI loss (vomiting, NG suction) due to assctd. urinary losses secondary to metabolic alkalosis and volume depletion (w/ volume depletion, aldosterone stimulates Na+ reabsorption and increases K+ secretion)
  • Lower GI loss (diarrhea)
  • Sweating
17
Q

HYPOK: What can cause renal loss of K+?

A
  • Diuretics (loop or thiazide)
  • Increased mineralcorticoid activity (aldosterone increases Na+ reabsorption via ENaC, so lumen becomes more neg, so more K+ secreted by ROMK)
  • Hypomagnesemia
  • RTA 1 or 2
  • Others
18
Q

HYPOK: What kind of cilia leads to increased K+ secretion

A

BENT

19
Q

HYPERK: What can cause transcellular shifts of K+?

A
  • PseudohyperK
  • Metabolic acidosis
  • Insulin deficiency, hyperglycemia, hyperosmolality
  • Increased tissue catabolism
  • Meds
  • Exercise
  • Transfusions
20
Q

How does insulin deficiency, hypergly, and hyperosmolality cause a transcellular shift leading to HYPERK?

A
  • Insulin stims. Na/K/ATPase to drive K+ intracellulary…so if you’re deficient, you aren’t driving K+ into the cell.
  • Hyperglycemia or hyperosmolality causes H2O to passively leave the cell and take K+ with it
21
Q

What kinds of things lead to increased tissue catabolism leading to a transcellular shift in HYPERK

A

Trauma, burns, radiation, tumor lysis syndrome, rhabdo

22
Q

What kinds of meds lead to transcellular shift in HYPERK

A

B2-blockers (remember, B2 helps drive K+ in…so if it’s blocked, get HYPERK)

aplha-1-adrenergic agonist (drives out; dopamine, phelyepherine, digoxin, succs, minoxidil)

23
Q

What 3 things can lead to pseudohyperK

A
  1. RBC hemolysis
  2. Serum blood samples- in thrombocytopenia, when the platelets clot it releases K. R/O w/ a plasma K+ (not clotted)
  3. Leukocytosis (fragile WBCs can rupture and leak K)
24
Q

HYPERK: What can lead to decreased renal K+ excretion/

A
  • Low aldosterone secretion
  • Aldosterone resistance (K+ sparing diuretics)
  • AKI or CKD
  • Hypovolemia
  • Ureterojejunostomy
  • Intrinsic renal defect
25
Q

What kinds of specific meds cause aldosterone resistance leading to decreased renal K+ excretion?

A

K+ sparing diuretics!

  • Aldosterone receptor blockers: spironolactone or eplerenone
  • Na channel blockers: amiloride or triamterene or trimethoprim
26
Q

How do you generally diagnose hyperK

A
  • Clinically
  • Labs guided by suspected cause given hx
  • FEK (<10% renal etiology, >10% extrarenal etiology)
  • DONT ORDER TTKG
27
Q

How do you prevent a bad arrhythmia in hyperK?

A

Give IV calcium gluconate

28
Q

How do you tx a transcellular shift in hyperK?

A
  • Insulin & Dextrose
  • B2 agonist: albuterol
  • Bicarb infusion
29
Q

How can you remove K+?

A

Slow: loop or thiazide diuretic or exhange resin (Kayexelate, zirconium, patiromer)

Fast: Hemodialysis

30
Q

How else can you tx hyperK?

A

Low K+ diet. Remove meds that increase K+ (ACEi/ARB, aldosterone blockers, K+ supplements)

31
Q

Def and RFs of HYPOK

A

Serum K<3.5 mEq/L

RFs: V/D, meds (diuretics, insulin, etc)

32
Q

Sx of HYPOK

A
  • Cardiac arrhytmia (PACs, PVCs, tachy, brady, vfib)
  • Skeletal muscle weakness (diaphragm!)
  • Rhabdo
  • Metabolic alkalosis (H+ enters ICF b/c K+ is leaving ECF in efforts to bump up K+ levels –> leads to not enough H+ in the ECF –> alkalosis)
  • Nephrogenic diabetes insipidus
33
Q

How does HYPOK affect RMP

A

Lowers it and makes it more negative. So it’s harder for an AP to occur due to hyperpolarization.

34
Q

WHat EKG changes are present in hypoK

A
  • Low T wave
  • Low T wave, high U wave
  • Low T wave, high U wave, low ST
35
Q

What are the 3 main reasons for HYPOK?

A
  1. Transcellular shift (cells uptake K)
  2. Extrarenal loss
  3. Renal loss
36
Q

How do you diagnose HYPOK?

A
  • Clinically
  • Labs guided by suspected cause given hx
  • Urinary K+ excretion to determine if it’s renal or extrarenal etiology
37
Q

How do you determine urinary K+ excretion when diagnosing HYPOK

A
  1. 24 hr urine K+. If >25-30/day = renal K wasting

2. Urine K/Cr ration. If higher value = renal K wasting

38
Q

How do you tx HYPOK

A
  • Tx underlying cause
  • Replace K+ deficit w/ KCL (K+ will increase by 0.1 for ever 10 mEq of KCl given)
  • Replace Mg if low
  • Repeat K+ labs

CPRII- Renal Exam (6 decks)

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