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M2 Renal/FEK > Potassium > Flashcards

Potassium Flashcards

1
Q

What is the most abundant cation in the body?

A

K, duh

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2
Q

What are the intra/extracellular concentrations of K?

A

intracellular [K] = 140mEq/L

extracellular [K] = 3.5 - 5mEq/L

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3
Q

What is the avg dietary intake of K? How does K change with each meal? What happens in patients with advanced kidney disease?

A

Average dietary K intake: 100-150mEq/d

(avg meal: 30-50mEq K avg ECFV is 14L but dietary K would acutely raise serum K by 2-3.5mEq/L after each meal (potentially fatal), but there are multiple mechanisms in place that prevent this acute rise

  • renal losses
  • GI losses

​Advanced kidney disease: GI losses are very important (can be 30-50% of daily dietary intake)

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4
Q

How does Na/K ATPase influence Na/K levels?

A

regulated by

  1. plasma K
  2. insulin
  3. exercise
  4. catecholamines
    • b2 -> hypokalemia
    • a2 -> hyperkalemia
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5
Q

How does catecholamines influence Na/K levels?

A

b2 -> incr. Na/K ATPase activity -> incr. K enters cells -> hypOkalemia

a2 -> decr. Na/K ATPase activity -> incr. K exit out of cells -> hypERkalemia

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6
Q

How does insulin influence Na/K levels?

What happens after meals?

What happens in insulin deficiency states?

A

insulin incr. Na/K ATPase activity -> incr. K uptake (maintains K within cells)

after a meal/during stress -> hypokalemia

insulin deficiency: no Na/K ATPase activity -> hyperkalemia

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7
Q

How does exercise influence Na/K levels?

A

exercise -> hyperkalemia due to K release into ECF from muscle cells -> vasodilation -> provide oxygen and energy to exercising muscles; can be deleterious if there is excess K release

ATP depletion -> decr. Na/K ATPase activity -> K diffuses out of cell

note: hyperkalemia is blunted in fit individuals

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8
Q

How does plasma K influence Na/K levels?

A

via H/K transporter

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9
Q

How does chronic kidney disease affect K levels?

A

Chronic diseases –> decr. Na/K ATPase activity

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10
Q

How does extracellular pH affect K levels?

A

low pH = H enters the cells, K exit to maintain electroneutrality

high pH = K enters the cells, H exits the cell

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11
Q

How does hyperosmolarity affect K levels?

A

Hyperosmolarity -> incr. K serum level

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12
Q

How does cell turnover affect K levels?

What about cell synthesis?

A

cell-turnover: breakdown -> incr. K release from cells -> hypERkalemia

cell-synthesis: hypOkalemia

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13
Q

How is K renally handled?

A

Normal GFR: 125cc/min -> 0.5mEq/min K is filtered; excretion can range from 1-80% of filtered K is freely filtered at the glomerulus

  • PCT: 67% reabsorbed passively
  • LOH: 20% reabsorbed via Na/K/2C by the time fluid reaches distal region, there is <10% filtered K remaining
  • DCT: can absorb 3% or secrete 50%
  • CCD: can absorb 9% by ICC cells or secrete 30% by principle cells
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14
Q

What is TTKG?

What are normal levels?

What does >11 mean?

What does <7 mean?

A

Transtubular K Gradient: TTKG = (UK x Sosm) / (SK x Uosm)

  • estimate ratio of K in the CCD lumen vs that in the peri-tubular capillaries
  • normal: 8-9
  • >11: hyperkalemia or high K intake (more K secreted into the urine)
  • <7: may indicate aldosterone deficit, esp if it is accompanied by hyponatremia + high urine Na
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15
Q

How does aldosterone affect kidney handling?

A
  • incr. K uptake into cells
  • incr. Na reabsorption/K secretion via luminal Na/K channels in principle cells (H2O follows)
    • As Na is reabsorbed, the tubular lumen becomes electronegative -> K enters the tubule to balance the charges)
  • incr. ENaC activity -> incr. Na uptake -
  • incr. Na/K ATPase on basal side

note: serum K is a potent stimulus of aldosterone

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16
Q

How does tubular flow rate affect K?

Hoes does ADH affect K?

A

As K enters the tubular lumen, there is a decreased electrochemical gradient for K secretion

high tubular flow rate -> K-free fluid from the proximal nephron will wash-out the high levels of luminal K -> decr. tubular K but incr. electrochemical gradient for K secretion -> incr secretion + hypokalemia

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17
Q

How does increased distal delivery of Na rate affect K?

What are some examples that do this?

A

If there are incr. Na in distal tubules (diuretics) -> incr. gradient for Na absorption -> incr. Na absorption -> tubular fluid becomes more electronegative, favoring K secretion

If Na absorption occurs through ENaC -> anion (Cl-) or excretion of cation (K) must occur to maintain electroneutrality!!

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18
Q

How does urinary anions affect K?

What are some examples that do this?

A

Non-resorbable anions (ex: ketoacids, HCO3, negatively-charged drugs/penicillin) -> incr. distal flow -> Na reabsorption occurs but the anions can’t be reabsorbed, so K has to be excreted to maintain electroneutrality -> hypokalemia + acidosis/metabolic

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19
Q

Hyperkalemia:

causes? (4)

manifestations? seriousness?

What is the first thing you should do?

A
  • incr K intake
  • decr. K excretion
  • transcellular shifts (cell -> ECF)
  • Spurious (pseudohyperkalemia)

manifestations: Asymptomatic, but life-threating ( can result in a cardiac arrest!!)

1st thing: EKG

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20
Q

What are the sx of hyperkalemia?

A
  • acute incr. K to 9 = medical emergency/fatal
  • slow incr. K to 9 = tolerated (ie chronic kidney dz); may not show EKG changes
  • cardiac arrhythmias
  • muscle weakness
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21
Q

What are the cardiac arrhythmia changes that you would see on a hyperkalemic patient from earliest to latest

A
  • Peaked T waves
  • QRS widening
  • PR prolongation
  • Loss of P wave
  • Sine wave / asystole
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22
Q

Why is hyperkalemia potentially fatal?

How is it treated?

A

HyperK -> lowers membrane potential -> persistent depolarization -> inactivation of VG Na channels -> EKG changes/arrhythmias

Trmt: Calcium - stabilizes the membranes and increase membrane excitability (reduced in hyperkalemia) -> resolution of QRS widening, presence of P waves, still observe T waves

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23
Q

First thing you should do with a patient with hyperkalemia?

A

GET EKG

confirm hyperkalemia if there are no EKG changes (repeat blood tests, minimize tourniquet time, use large needle for phlebotomy)

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24
Q

How do you manage a patient with ACUTE hyperkalemia?

A

ACUTE Hyperkalemia: medical emergency/fatal

  • IV Ca if EKG changes
  • Insulin/glucose/dextrose or albuterol once patient is stabilized
  • Bicarbonate if acidosis is present
  • Kayexalate; repeat doses based on initial K+ level
  • Stop offending medications; optimize renal function
  • Dialysis only if K >7 or QRS widening with renal failure, inability to use Kayexalate, or ongoing K release (GI bleed, increased cell turnover/tumor lysis)
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25
Q

How do you manage a patient with CHRONIC hyperkalemia?

A

remember, they are the ones tolerated (ie chronic kidney dz) and may not show EKG changes

  • CHRONIC HYPERKALEMIA
  • Fludrocortisone if no HTN and no fluid overload
  • Furosemide if fludrocortisone is contraindicated
  • Low K+ diet
  • Avoid provoking medications (NSAIDS, ACEI, ARB, K+-sparing diuretics)
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26
Q

Hypokalemia:

causes? (4)

manifestations? seriousness?

What is the first thing you should do?

A

Causes

  • decr. K intake
  • incr. K losses (renal, GI/extrarenal)
  • trasnscellular shifts (ECF -> cell)
  • Spurious (pseudohyperkalemia)

Most common Symptomatic, but rarely life-threatening

KCl replacement salt, unless significant acidosis is present
but avoid dextrose solution

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27
Q

What are the clinical manifestations of hypokalemia?

A
  • muscle weakness (due to increased membrane excitability)
  • Cardiac arrhythmias (due to altered resting membrane potential and repolarization)
  • Metabolic alkalosis (hypokalemia -> renal H+ secretion)
  • Nephrogenic diabetes insipidus (mxn not entirely clear, may be due to increased thirst and impaired ability to concentrate urine, incr. AQP2 channelsg -> H2O reabsorption)
  • Rhabdomyolysis
  • Kaliopenic nephropathy (tubular interstitial scarring, fibrosis, cyst formation, etc)
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28
Q

How do you manage hypokalemic patients?

A
  • KCl replacement salt, unless significant acidosis is present
    • avoid dextrose solutions - these will stimulate insulin release, which will induce intracellular shift of K, exacerbating hypokalemia!
    • Maximal peripheral vein tolerance = 60 mEq/L K; doses greater than this should be given through central vein (femoral) to avoid CHF
    • Monitor with ECG if administration is >10mEq/h
  • Correct alkalosis when possible
  • Dialysis in severe patients
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29
Q

4 causes of hyperkalemia

A
  • increased K intake
  • decreased K excretion
  • Transcellular K Shifts
  • Spurious (pseudohyperkalemia)
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30
Q

How does increased intake cause hyperkalemia? 3

A

If patient has normal renal handling, the body can handle large dietary loads of K and not get hyperkalemia; dietary loads are only significant with decreased renal excretion and can have a negative impact on health

Medications that increase K (antibiotics, K supplements)

Replacement salt (KCl)

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31
Q

How does hyerkalemia prevented in renal insufficiency?

What mediates these? (2)

When does hyperkalemia set in?

A

K balance is maintained in renal failure by increased excretion by functioning nephrons, which undergo hypertrophy to take over K handling and other functions as well).

This is effectively mediated by aldosterone, Na/K ATPase only if there is normal urine output.

If oliguria sets, adaptive mechanisms are insufficient and patient begins to retain K.

32
Q

What 3 channels does Aldosterone affect?

How does hypOaldosteronism result in hyperkalemia?

A
  1. ENaC
  2. NA/K ATPase
  3. H channel

No aldosterone OR aldosterone resistance -> Na channels in CD affected -> inability to generate negative electrical gradient for K secretion

33
Q

What are some primary causes of no aldosterone? (3)

A

adrenal gland damage (Addisonian crisis) due to autoimmune, shock, sepsis, hemorrhage; characterized by hypotension, fatigue, malaise, hyperkalemia, abdominal pain

  • *congenital (21-hydroxylase deficiency)**
  • *heparin** (see meds)
34
Q

What are some secondary causes of no aldosterone? (3)

A
  • Hyporeninemic Hypoaldosteronism – JG damage, diabetic neuropathy, obstructive uropathy, chronic interstitial nephritis, oliguric failure
  • ACEi/ARB therapy (see meds)
35
Q

What are 3 mechanisms of Aldosterone resistance?

A
  • PHA-I AR – very severe, extrarenal manifestations at all organ sites; requires lifelong salt therapy
  • PHA-I AD – milder form, limited to kidney only; resolves with age
  • PHA-II – Gordon’s Syndrome “familial hyperkalemic HTN” caused by WNK disorders; trmt: thiazides
36
Q

How does ACEI/ARB affect K balance?

A

decr. AII -> decr. aldosterone production + efferent arteriole dilation -> decr. GFR -> decr. tubular flow rate

37
Q

How does heparin affect K balance?

A

blocks aldosterone production; reversible

38
Q

How does K sparing diuretics affect K balance?

A

Inhibits Na+ reabsorption in DCT -> inability to generate negative electrical gradient for K+ secretion.

Examples: Amiloride, Triamterene, Spironolactone, Eplernone

39
Q

How does NSAIDs affect K balance?

A
  • NSAIDs cause interstitial nephritis (direct tubular damage) -> decr. renin -> hypoaldosterone state
  • NSAIDs also cause afferent arteriolar constriction (due to decr. prostaglandin synthesis) -> decr. GFR -> ischemic tubular damage + decr. tubular flow rate (-> decr. electrochemical gradient)
40
Q

How does Cyclosporine affect K balance?

A

dose-dependent afferent arteriolar vasoconstriction -> decr. GFR (manifested as incr. serum creatinine) + ischemic tubular damage -> decr. tubular flow rate

41
Q

How does bactrim affect K balance?

A

trimethoprim is structurally similar to K sparing diuretics and it blocks the Na channels in the DCT -> decr. Na reabsorption -> decr. electrical gradient for K secretion

42
Q

How does cell death affect K balance?

A

release intracellular K

ATP depletion also decreases Na/K ATPase activity -> K diffuses out of cell -> hyperkalemia

43
Q

How does digitalis affect K balance?

A

Directly inhibits Na/K ATPase activity -> K diffuses out of cell

44
Q

How does Succinylcholine affect K balance?

A

causes depolarization of AChR -> potassium efflux from the muscle

45
Q

How does Hyperosmolarity affect K balance?

A

H2O exits cells -> incr. intracellular K concentration -> K diffuses out of cells -> hyperkalemia

Solvent drag: large quantities of H2O drags K out into ECF as it exits the cell

46
Q

What is Spurious hypperkalemia?

A

pseudohyperkalemia caused by

  • severe leukocytosis /thrombocytosis -> K is released from cells
  • Hemolyzed blood sample (ie blood drawn through a narrow needle
  • Prolonged tourniquet time -> promotes trauma to cells g K release
47
Q

What are 4 main causes of hypokalemia? (5)

A
  • decreased K intake
  • increased K excretion
  • increased GI losses
  • transcellular shifting
  • spurious
48
Q

How does decreased K intake affect K balance?

A

Pure dietary K deficiency is rare

49
Q

how does diuretics affect K balance?

A

Loop diuretics can cause hypokalemia less often than thiazides (maybe due to shorter half-life)

50
Q

In what situation would you find incr. renin + incr. aldo production? 3

A
  • renin producing tumors
  • extrinsic compression, hematoma
  • RAS -> decr. GFR -> decr. Na delivery to distal tubule -> JG responds as if its in a volume depleted state
51
Q

In what situations would you find decr. renin + incr. aldo? 3

A
  • adrenal adenoma – excess aldosterone production (1˚)
  • bilateral adrenal hyperplasia
  • glucocorticoid remediable aldosteronism (GRA) – due to cross-over of genes that form aldosterone (zona glomerulosa) and glucocorticoids (zona fasciculata) that results in abnormal chimeric genes g ectopic aldosterone synthase activity in the cortisol-producing zona fasciculata of the adrenal cortex, under the regulation of adrenocorticotropin (ACTH)
    • trmt: dextamethasone to suppress aldosterone production
52
Q

What is glucocorticoid remediable aldosteronism (GRA)? 3

A

cross-over of genes that form aldosterone (zona glomerulosa) and glucocorticoids (zona fasciculata) that results in abnormal chimeric genes g ectopic aldosterone synthase activity in the cortisol-producing zona fasciculata of the adrenal cortex, under the regulation of adrenocorticotropin (ACTH)

trmt: dextamethasone to suppress aldosterone production

53
Q

In what situation would you find decr. renin + decr. aldosterone? 3

A
  • Cushings
  • Syndrome of apparent mineralcorticoid excess - mutation in 11β-HSD -> increased cortisol levels -> activation of mineralocorticoid receptor -> aldosterone like effects in the kidney
    • 11β-HSD normally activates cortisol -> cortisone
  • Liddle’s syndrome - activating ENaC mutation -> incr. Na reabsorption -> volume expansion -> HTN with decr. renin, decr. aldosterone, metabolic alkalosis, and hypokalemia
    • trmt: block ENaC
54
Q

How does anion excess in the tubular lumen affect K balance?

What are some examples of anions?

A

HCO3-, ketones, toluene (glue), penicillins

To maintain neutroality -> k is excreted -> hypokalemia

55
Q

How does polyuria affect K balance?

A

Significant polyuris (>5L/day) -> incr. distal flow rates -> washes out K out of CD lumen and replaces it with “K-free” fluid from the proximal tubule, which decr. electrochemical gradient -> favors excretion of K into the tubule

56
Q

how does Hypomagnesemia affect K balance?

What are some causes of hypoMg?

A
  • causes renal K wasting via ROMK channels
  • Causes: diuretics, vomiting, diarrhea
  • Correction of hypokalemia is often impossible until hypomagnesemia is corrected
57
Q

Bartter’s dz mutation?

What is the effect of this mutation?

A

inactivating mutation in Na/K/2Cl pump in TALH

body behave as if chronically on loop diuretics

net effects: hypokalemia, hypomagnesemia, metabolic alkalosis, hypercalciuria, volume depletion

58
Q

Gittleman’s dz mutation?

What is the effect of this mutation?

A

inactivating mutation in the NaCl cotransporter in the DCT

patients behave as if chronically on thiazide diuretics

Characterized by: hypokalemia, hypomagnesemia, metabolic alkalosis, hypocalciuria, and normal BP

59
Q

Liddle’s dz mutation?

What is the net effect of this mutation?

A

Activating ENaC mutation in

body behaves like it has volume expansion (HTN associated with decr. renin, decr. aldosterone, metabolic alkalosis, hypokalemia)

trmt: block ENaC

60
Q

How does diarrhea, diuretics, or laxatives affect K balance?

A

volume depletion –> increase aldosterone levels

leads to incr. Na reabsorption in DCT + incr. K/H secretion

61
Q

How does Gastric Losses (vomiting) affect K balance?

A
  • Vomiting -> H+ losses -> metabolic alkalosis -> incr. HCO3 excretion, which acts as an unreabsorbed anion in the urine -> draws K into the lumen to maintain electroneutrality
  • Volume depletion -> incr. aldosterone production -> K excretion
62
Q

What causes Hyperinsulinemia (3) and how does this affect K balance?

A
  • Insulinomas, rare
  • Insulin overdoses in diabetic patients, common
  • Insulin infusions for diabetic ketoacidosis

cause hypOkalemia

63
Q

What are the causes of adrenergic excess? (4)

how does this affect K balance?

A
  • Pheochromocytoma, rare
  • Overuse of b-2 agonists in COPD, common
  • Anxiety -> hyperventilation -> incr pH -> intracellular K shift + extracellular H shift -> decr. pH
  • high adrenergic output -> favors intracelluar K+ shifting
64
Q

How does alkalemia affect K balance??

A
  • incr. pH -> K shift into cells
  • kidneys attempt to correct alkalemia by excreting HCO3
  • Bicarbonaturia leads to urinary K+ wasting b/c K+ remains in the urine to balance the charge of HCO3
65
Q

How does Refeeding Syndrome cause hypokalemia?

A

feeding a chronically starved patient (total body deficit of electrolytes) -> insulin + catecholamine release -> increased intracellular shift of K and unmask a hypokalemia

“Patient comes in with normal electrolytes, then fed, then electrolytes become low”

66
Q

how does incr. RBC production/rapid cell growth affect K balance?

A
  • Rapid cell growth consumes K+
  • Fast growing malignancies such as leukemias can utilize large amounts of K+
  • Refeeding after starvation can lead to rapid cell growth in a K+-depleted individual (postprandial insulin release exacerbates hypokalemia)
67
Q

How can periodic paralysis affect K balance?

A
  • Rare genetic disorder that results in recurrent severe hypokalemia and paralysis (secondary to the i K)
  • Acquired disorder is associated with thryotoxicosis in Asian males (mxn unknown)
  • Hypokalemia often triggered by exercise, stress, or eating
  • K+ can transiently drop below 2
68
Q

What causes Spurious Hypokalemia?

A
  • severe leukocytosis (actively metabolic cells) -> incr. cellular uptake of K -> hypokalemia
  • avoided by rapid refrigeration and sample processing
69
Q

Why is Ca used as a 1st line trmt for hyperkalemia?

does it affect K levels?

A

Stabilizes myocardial membrane by increasing membrane excitability

1st STEP Tx for EKG CHANGES

does not affect K levels

70
Q

Why is insulin/glucose used as a treatment for hyperkalemia?

does it affect K levels?

A

Insulin incr. Na/K ATPase activity -> incr K uptake into cells

TEMPORARY Tx

Yes - it decr. serum K by 1-2mEq but does not remove K from the body

71
Q

Why is bicarbonate used as a treatment for hyperkalemia?

does it affect K levels?

A

Only effective in patients with metabolic acidosis (serum bicarbonate <20)

TEMPORARY Tx

decr. serum K, by 1-2mEq but does not remove K from the body

72
Q

Why is albuterol used as a treatment for hyperkalemia?

does it affect K levels?

A

b2 activation -> incr. Na/K ATPase activity -> incr. K entery into cells -> hypokalemia

TEMPORARY Tx

73
Q

Why is Kayexalate used as a treatment for hyperkalemia?

does it affect K levels?

A

Exchanges K for Na in the GI

Caution in CHF or patients with end-stage renal disease due to risk of volume overload

LONG-term Tx

Lowers serum K

74
Q

What are some short-term trmts for hyperkalemia?

A
  • Calcium
  • Insulin/Glucose or dextrose
  • Bicarbonate
  • Albuterol
75
Q

Long-term treatments for hyperkalemia?

A

Kayexalate

M2 Renal/FEK (20 decks)

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