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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
How do you manage a patient with CHRONIC hyperkalemia?
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)
26
Hypokalemia: causes? (4) manifestations? seriousness? What is the first thing you should do?
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**
27
What are the clinical manifestations of hypokalemia?
* 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)
28
How do you manage hypokalemic patients?
* 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
29
4 causes of hyperkalemia
* increased K intake * decreased K excretion * Transcellular K Shifts * Spurious (pseudohyperkalemia)
30
How does increased intake cause hyperkalemia? 3
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)**
31
How does hyerkalemia prevented in renal insufficiency? What mediates these? (2) When does hyperkalemia set in?
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
What 3 channels does Aldosterone affect? How does hypOaldosteronism result in hyperkalemia?
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
What are some primary causes of no aldosterone? (3)
**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
What are some secondary causes of no aldosterone? (3)
* Hypo**renin**emic Hypo**aldosteronism** – JG damage, diabetic neuropathy, obstructive uropathy, chronic interstitial nephritis, oliguric failure * ACEi/ARB therapy (see meds)
35
What are 3 mechanisms of Aldosterone resistance?
* 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
How does ACEI/ARB affect K balance?
decr. AII -\> decr. aldosterone production + efferent arteriole dilation -\> decr. GFR -\> decr. tubular flow rate
37
How does heparin affect K balance?
blocks aldosterone production; reversible
38
How does K sparing diuretics affect K balance?
Inhibits Na+ reabsorption in DCT -\> inability to generate negative electrical gradient for K+ secretion. Examples: Amiloride, Triamterene, Spironolactone, Eplernone
39
How does NSAIDs affect K balance?
* 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
How does Cyclosporine affect K balance?
dose-dependent **afferent arteriolar vasoconstriction** -\> decr. GFR (manifested as incr. serum creatinine) + ischemic tubular damage -\> decr. tubular flow rate
41
How does bactrim affect K balance?
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
How does cell death affect K balance?
release intracellular K ATP depletion also decreases Na/K ATPase activity -\> K diffuses out of cell -\> hyperkalemia
43
How does digitalis affect K balance?
Directly inhibits Na/K ATPase activity -\> K diffuses out of cell
44
How does Succinylcholine affect K balance?
causes depolarization of AChR -\> potassium efflux from the muscle
45
How does Hyperosmolarity affect K balance?
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
What is Spurious hypperkalemia?
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
What are 4 main causes of hypokalemia? (5)
* decreased K intake * increased K excretion * increased GI losses * transcellular shifting * spurious
48
How does decreased K intake affect K balance?
Pure dietary K deficiency is rare
49
how does diuretics affect K balance?
Loop diuretics can cause hypokalemia less often than thiazides (maybe due to shorter half-life)
50
In what situation would you find incr. renin + incr. aldo production? 3
* 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
In what situations would you find decr. renin + incr. aldo? 3
* 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
What is glucocorticoid remediable aldosteronism (GRA)? 3
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
In what situation would you find decr. renin + decr. aldosterone? 3
* 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
How does anion excess in the tubular lumen affect K balance? What are some examples of anions?
HCO3-, ketones, toluene (glue), penicillins To maintain neutroality -\> k is excreted -\> hypokalemia
55
How does polyuria affect K balance?
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
how does Hypomagnesemia affect K balance? What are some causes of hypoMg?
* causes renal K wasting via ROMK channels * Causes: diuretics, vomiting, diarrhea * Correction of hypokalemia is often impossible until hypomagnesemia is corrected
57
Bartter’s dz mutation? What is the effect of this mutation?
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
Gittleman’s dz mutation? What is the effect of this mutation?
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
Liddle’s dz mutation? What is the net effect of this mutation?
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
How does diarrhea, diuretics, or laxatives affect K balance?
volume depletion --\> increase aldosterone levels leads to incr. Na reabsorption in DCT + incr. K/H secretion
61
How does Gastric Losses (vomiting) affect K balance?
* 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
What causes Hyperinsulinemia (3) and how does this affect K balance?
* Insulinomas, rare * Insulin overdoses in diabetic patients, common * Insulin infusions for diabetic ketoacidosis cause hypOkalemia
63
What are the causes of adrenergic excess? (4) how does this affect K balance?
* 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
How does alkalemia affect K balance??
* 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
How does Refeeding Syndrome cause hypokalemia?
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
how does incr. RBC production/rapid cell growth affect K balance?
* 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
How can periodic paralysis affect K balance?
* 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
What causes Spurious Hypokalemia?
* severe leukocytosis (actively metabolic cells) -\> incr. cellular uptake of K -\> hypokalemia * avoided by rapid refrigeration and sample processing
69
Why is Ca used as a 1st line trmt for hyperkalemia? does it affect K levels?
Stabilizes myocardial membrane by increasing membrane excitability 1st STEP Tx for EKG CHANGES does not affect K levels
70
Why is insulin/glucose used as a treatment for hyperkalemia? does it affect K levels?
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
Why is bicarbonate used as a treatment for hyperkalemia? does it affect K levels?
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
Why is albuterol used as a treatment for hyperkalemia? does it affect K levels?
b2 activation -\> incr. Na/K ATPase activity -\> incr. K entery into cells -\> hypokalemia TEMPORARY Tx
73
Why is Kayexalate used as a treatment for hyperkalemia? does it affect K levels?
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
What are some short-term trmts for hyperkalemia?
* Calcium * Insulin/Glucose or dextrose * Bicarbonate * Albuterol
75
Long-term treatments for hyperkalemia?
Kayexalate

M2 Renal/FEK (20 decks)

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